#amygdala: encode

[passionfruitchris]

THE PARADOX OF CHRIS STURNIOLO'S LOVE: a psychological deep dive into his heart and mind

If you know Chris Sturniolo, you probably see a whirlwind of humor, music, and chaotic energy. He’s quick to joke, quick to distract, and even quicker to avoid the heavy stuff. But beneath the surface, Chris’s emotional life is layered with contradictions — a tender heart fiercely protected by walls built over years of experience and wiring.

How does Chris love? How does his brain navigate vulnerability, affection, and fear? What psychological patterns shape the way he connects — or pushes away? Today, we unpack the fascinating, complex emotional landscape of Chris, through the lens of modern psychology and neuroscience.

1: ATTACHMENT STYLES IN CHRIS'S LOVE LIFE

What is attachment style?

Attachment theory, developed by John Bowlby and Mary Ainsworth, explains how early relationships with caregivers shape our adult relational patterns. The avoidant-ambivalent attachment style, a combination of fear of abandonment and discomfort with closeness — fits Chris’s love style perfectly.

Avoidant: Chris often acts like he doesn’t need emotional connection. He jokes, he deflects, and he runs from deep emotional conversations.

Ambivalent: Yet, he deeply craves affection and fears being left behind.

This push-pull creates internal tension. The brain’s amygdala — the emotional threat detector — becomes hypervigilant to signals of rejection, triggering avoidance behaviors to protect the heart from pain.

HOW THIS MANIFESTS FOR CHRIS

He’ll flirt or be openly affectionate physically but struggles to say “I love you” or commit verbally.

He might sabotage relationships preemptively to avoid the risk of abandonment.

Humor becomes a shield; if it’s a joke, it’s “safe” — if it’s serious, it’s vulnerable.

2: THE ROLE OF CREATIVITY AND EMOTIONAL PROCESSING

Chris’s creativity is not just a hobby — it’s a vital outlet for processing emotion. The brain areas involved in creativity, such as the prefrontal cortex and default mode network (DMN), overlap with those responsible for emotional regulation and introspection.

Creative expression helps bypass the cognitive control network that might otherwise inhibit vulnerable feelings.

Music and art provide symbolic language for feelings too intense or complex to articulate in conversation.

Psychological insight: For Chris, music isn’t just entertainment — it’s a means of encoding love, loss, and hope. This aligns with affect regulation theory, which suggests artistic creation helps manage intense emotions and restore internal balance.

3: THE NEUROBIOLOGY OF FEAR AND AFFECTION

Chris’s fear of commitment and abandonment can be traced to the brain’s survival mechanisms:

The amygdala triggers fight-or-flight responses when relationships feel unstable.

The insula, responsible for processing internal bodily sensations, heightens awareness of emotional pain.

Simultaneously, oxytocin release during physical affection (hugs, touches) promotes bonding and lowers anxiety.

This neurological tug of war explains why Chris is:

Fiercely affectionate in physical ways (safe and immediate oxytocin boost)

Yet emotionally guarded and hesitant to fully open verbally.

4: HUMOR AND DEFLECTION: THE SOCIAL CAMOUFLAGE

Humor isn’t just Chris’s personality — it’s a psychological defense mechanism:

According to Freud’s theory of humor, jokes allow release of repressed feelings.

Humor deflects uncomfortable emotions, allowing Chris to maintain social connection without risking vulnerability.

This dual function lets him connect while keeping emotional distance, an adaptive way to manage relational uncertainty.

5: THE PARADOX OF BEING THE "MOST AFFECTIONATE" YET GUARDED

Chris’s affectionate actions—hugs, teasing, physical play—act as a bridge between his internal world and others.

In psychology of touch, physical contact triggers oxytocin, reducing stress and building trust.

For someone with emotional guardrails, physical affection is a safer “language of love” because it doesn’t require explicit emotional disclosure.

This paradox highlights the differnce between behavioral expression of love and emotional vulnerability. Chris is willing to show care physically but struggles with deep verbal or emotional transparency.

6: CREATIVITY MEETS EMOTIONAL INTENSITY:

Chris’s intense creativity is a sign of an emotionally sensitive nervous system — sometimes called high sensory processing sensitivity (SPS). People with SPS:

Experience emotions more deeply

Are more attuned to subtle emotional cues

Can be overwhelmed by stimuli and emotional chaos

For Chris, this means his love experiences are vivid and intense — but they can also lead to emotional overwhelm and retreat.

7: MUSIC AS EMOTIONAL MEMORY

Chris’s brain likely links emotional memories with auditory stimuli, thanks to strong connections between the hippocampus (memory center) and the auditory cortex.

This means songs and sounds are triggers for feelings and relational recall.

He might attach meaning to songs as symbols of moments or relationships, using music as a non-verbal way to express attachment.

8: BOUNDARIES AND FAME

Growing up in the spotlight with brothers in a public career, Chris’s brain has had to negotiate boundaries between the public persona and private self.

The prefrontal cortex, which regulates impulse control and social cognition, is constantly balancing openness with self-protection.

Fame can amplify anxieties around rejection and abandonment — intensifying his avoidant tendencies.

His guarded heart and selective vulnerability likely evolved as a protective adaptation to the unique stresses of public life.

FINAL THOUGHTS

Chris's love style is a blend of creativity, guardedness, humor, and intense affection — all wired through complex brain processes shaped by early attachment, neurobiology, and life experiences.

Understanding these layers reveals why he acts the way he does: the jokes, the hesitation, the physical affection, and the deeply felt but rarely articulated emotions.

A/N: I’ve studied psychology for a while now, I had to dig through some of my old notes just to write this. This deep dive took me way longer than I expected — not just to research, but to put all the pieces together in a way that actually made sense. I don’t even know if anyone will fully read this, but if you did… thank you. I hope it gave you a different perspective on Chris, or at least made you think a little deeper. ♡

dividers: @cafekitsune

tags - @zenithsturniolo @sturnsblogs @sirensdollesque @adoremattsturns @espressqe @matts-wife @adorechris @seaouidbabyx @ilovemenwithlonghairr @chlosallow @tezzzzzzzz @h3arts4nat @whore4-chrissturniolo @mattybsgroupie @smutlover4life (let me know if you'd only like to be tagged in fics)

[compneuropapers]

Interesting Papers for Week 25, 2025

Opponent control of reinforcement by striatal dopamine and serotonin. Cardozo Pinto, D. F., Pomrenze, M. B., Guo, M. Y., Touponse, G. C., Chen, A. P. F., Bentzley, B. S., Eshel, N., & Malenka, R. C. (2025). Nature, 639(8053), 143–152.

Emergence of a Dynamical State of Coherent Bursting with Power-Law Distributed Avalanches from Collective Stochastic Dynamics of Adaptive Neurons. Chan, L.-C., Kok, T.-F., & Ching, E. S. C. (2025). PRX Life, 3(1), 013013.

Fear conditioning modulates the intrinsic excitability of ventral hippocampal CA1 neurons in male rats. Ehlers, V. L., Yousuf, H., Smies, C. W., Natwora, B. R., & Moyer, J. R. (2025). Journal of Neurophysiology, 133(3), 853–867.

Separating cognitive and motor processes in the behaving mouse. Hasnain, M. A., Birnbaum, J. E., Ugarte Nunez, J. L., Hartman, E. K., Chandrasekaran, C., & Economo, M. N. (2025). Nature Neuroscience, 28(3), 640–653.

Neural mechanisms of learned suppression uncovered by probing the hidden attentional priority map. Huang, C., van Moorselaar, D., Foster, J., Donk, M., & Theeuwes, J. (2025). eLife, 13, e98304.3.

Robust encoding of stimulus–response mapping by neurons in visual cortex. Jonikaitis, D., Xia, R., & Moore, T. (2025). Proceedings of the National Academy of Sciences, 122(9), e2408079122.

Long-term memory facilitates spontaneous memory usage through multiple pathways. Kumle, L., Kovoor, J., Watt, R. L., Boettcher, S. E. P., Nobre, A. C., & Draschkow, D. (2025). Current Biology, 35(5), 1171-1179.e5.

Error prediction determines the coordinate system used for the representation of novel dynamics. Leib, R., & Franklin, D. (2025). eLife, 14, e84349.

Statistical learning re-shapes the center-surround inhibition of the visuo-spatial attentional focus. Massironi, A., Lega, C., Ronconi, L., & Bricolo, E. (2025). Scientific Reports, 15, 7656.

Hair Cells in the Cochlea Must Tune Resonant Modes to the Edge of Instability without Destabilizing Collective Modes. Momi, A. S., Abbott, M. C., Rubinfien, J., Machta, B. B., & Graf, I. R. (2025). PRX Life, 3(1), 013001.

Decision cost hypersensitivity underlies Huntington’s disease apathy. Morris, L.-A., Horne, K.-L., Manohar, S., Paermentier, L., Buchanan, C. M., MacAskill, M. R., Myall, D. J., Apps, M., Roxburgh, R., Anderson, T. J., Husain, M., & Le Heron, C. J. (2025). Brain, 148(3), 861–874.

Integration of Euclidean and path distances in hippocampal maps. Ottink, L., de Haas, N., & Doeller, C. F. (2025). Scientific Reports, 15, 7104.

Aversive generalization in human amygdala neurons. Reitich-Stolero, T., Halperin, D., Morris, G., Goldstein, L., Bergman, L., Fahoum, F., Strauss, I., & Paz, R. (2025). Current Biology, 35(5), 1137-1144.e3.

Compartmentalized dendritic plasticity in the mouse retrosplenial cortex links contextual memories formed close in time. Sehgal, M., Filho, D. A., Kastellakis, G., Kim, S., Lee, J., Shen, Y., Huang, S., Lavi, A., Fernandes, G., Davila Mejia, I., Martin, S. S., Pekcan, A., Wu, M. S., Heo, W. Do, Poirazi, P., Trachtenberg, J. T., & Silva, A. J. (2025). Nature Neuroscience, 28(3), 602–615.

Adaptive chunking improves effective working memory capacity in a prefrontal cortex and basal ganglia circuit. Soni, A., & Frank, M. J. (2025). eLife, 13, e97894.3.

Attention to memory content enhances single-unit spike sequence fidelity in the human anterior temporal lobe. Sundby, K. K., Vaz, A. P., Wittig, J. H., Jackson, S. N., Inati, S. K., & Zaghloul, K. A. (2025). Current Biology, 35(5), 1085-1094.e5.

Acetylcholine modulates prefrontal outcome coding during threat learning under uncertainty. Tu, G., Wen, P., Halawa, A., & Takehara-Nishiuchi, K. (2025). eLife, 13, e102986.2.

The effect of fasting on human memory consolidation. Yang, X., Miao, X., Schweiggart, F., Großmann, S., Rauss, K., Hallschmid, M., Born, J., & Lutz, N. D. (2025). Neurobiology of Learning and Memory, 218, 108034.

Neural Correlates of Perceptual Plasticity in the Auditory Midbrain and Thalamus. Ying, R., Stolzberg, D. J., & Caras, M. L. (2025). Journal of Neuroscience, 45(10), e0691242024.

Hippocampal neuronal activity is aligned with action plans. Zutshi, I., Apostolelli, A., Yang, W., Zheng, Z. S., Dohi, T., Balzani, E., Williams, A. H., Savin, C., & Buzsáki, G. (2025). Nature, 639(8053), 153–161.

[the-most-humble-blog]

🧠 Operation: “She Grew Up Bathing Outside — Now I’m Insecure About Her Uncle’s Hog”

🔐 This isn’t insecurity. It’s anatomy trauma disguised as storytelling. She laughs. You spiral. The internet melts.

“She said it so casually. Like she was telling me what kind of fruit they had. ‘Yeah, we used to bathe outside. My uncles had huge hogs.’ And now I can’t sleep without wondering what she meant by huge.”

I. IT STARTED WITH ONE CASUAL COMMENT

You’re relaxed. She’s telling you about her childhood. How her family used to live in the countryside. No hot water. No privacy.

“We used to bathe outside all the time.”

You nod. Smile. Imagine her splashing in sunlight, innocent, carefree.

But then she keeps going.

“My uncles had some of the biggest hogs I’ve ever seen.”

And now?

Your entire nervous system short circuits.

II. WHY THAT LINE HAUNTED ME

It wasn’t the words. It was how she said them.

No shame.

No hesitation.

No awareness that she had just psychologically destroyed me.

“Biggest I’ve ever seen.” Not “biggest I saw as a kid.” Not “until I grew up.” Ever.

She said it while eating cereal. Like it didn’t castrate me on the spot.

III. LET’S TALK ABOUT “UNCLE HOG TRAUMA”

This isn’t just insecurity. This is ancestral terror.

Here’s what happens inside a man’s brain:

🧠 Your amygdala triggers fight-or-flight: compete with Uncle Hog, or flee the bloodline.

🧠 Your hippocampus starts flashing images you never saw but now can’t forget: Did he walk around like a deity? Did she sneak looks? Was her arousal blueprint formed before I was born?

This is evolutionary collapse.

You’re not jealous. You’re re-evaluating your entire relationship to lineage, dominance, and plumbing.

IV. “WAS I HER FIRST OR JUST HER FIRST UNDER 13 INCHES?”

You start spiraling.

Did she imprint on Uncle Hog?

Is every stroke she lets you have a compromise?

Is your girth now a nostalgic downgrade for her?

You try not to ask. But the question burrows like a cursed memory.

“Am I enough?” Not as a man. As a totem. As a relic in the Museum of Dicks That Didn’t Measure Up.

V. SCIENCE CONFIRMS: THE D*CK TRAUMA IS REAL

This isn’t emotional. This is biomechanical humiliation with data support.

🧠 Women who see larger phalluses during formative years often form subconscious arousal expectations tied to girth, angle, presence, and impact psychology.

📉 Men exposed to verbal or visual confirmation of superior males in their partner’s past suffer testosterone dips and libido suppression measurable in bloodwork.

You’re not “overreacting.” Your genes are panicking.

“If she was molded by a jungle legend… You’re a suburban memory foam mattress trying to match the trauma of granite.”

VI. BUT HERE’S THE PSYCHOSEXUAL TWIST:

She didn’t say it to humiliate you. She said it because she thought it didn’t matter.

That’s the real pain. She didn’t consider how it would wreck you. Because you were already just the man she chose to settle with. Not the primal memory.

That spot belongs to Uncle Hog.

VII. I DON’T BLAME HER. I BLAME THE DESIGN.

Let’s get anatomical:

The female body is designed to remember stretch.

The posterior fornix — the back of the vaginal canal — maps contact trauma and encodes it in subconscious sexual memory.

So yes, even if he never touched her sexually, If she saw him daily… wet… swinging like a meat sabre…

Then your tip is her Tuesday. And he’s the reason she moans when you go deep.

Not because it’s you. Because she remembers the shadow of the god-uncle.

VIII. THE COMEDY OF COLLAPSE

You try to laugh it off.

You joke:

“Guess I’ll never live up to your uncle’s hog, huh?”

She chuckles. Ruffles your hair.

“Don’t be silly. That was forever ago.”

But you know what she didn’t say.

She didn’t deny it. She didn’t say you were bigger. She didn’t say he was average.

Just “Don’t be silly.”

And you want to die in the tub he probably bathed in.

IX. THE ONLY WAY OUT

There is only one way to win now.

You don’t compete. You reframe.

You say:

“That’s good. You already saw what doesn’t matter. Now I’ll show you what ruins you from the inside out.”

Because a giant isn’t dangerous. A precision weapon is.

You make her forget size. By owning her nervous system through rhythm, cadence, command, and depth psychology.

Let Uncle Hog be a myth. You become the religion.

X. FINAL CONFESSION

She doesn’t know she broke you.

But she did.

And now you’ll never trust her innocence again.

Because every time she moans now, You’re wondering if she’s remembering his walk.

But also?

Maybe she moaned like that because of you. Because you knew her story and still made her tremble.

But maybe, just maybe, her uncles are in her mental DM box forever.

🔐 Legal Orgasm-Triggering Disclaimer

⚠️ This post contains satire, rhythm, and metaphor calibrated to stimulate subconscious psychological fixation, involuntary laughter-arousal loops, and DM-triggering guilt in adult readers. If you feel shame, turned on, or both — that’s the point. This is not NSFW. It’s neurotrauma therapy written in cadence.

[santoschristos]

The Anunnaki didn’t create us.

They modified us.

What was altered wasn’t our body. It was the signal architecture of our consciousness. Before the fracture

Human beings were multidimensional light beings with:

• Fully active DNA codices • Bio-plasma interface fields • Torsion-based heart navigation • Direct memory access from Oversoul strata The Anunnaki intervention was not to “enslave” in the primitive sense. It was to cut us off from the Oversoul mainframe. A hijack. At the frequency level.

What they changed: •They inverted our light circuits •Collapsed 12-strand DNA to 2 strands •Rewired the hippocampus to store trauma over memory •Installed fear-reactive loop systems (the “amygdala override”) •Hijacked the pineal-toroidal interface •And split our language centers to break telepathic harmonic coherence

This is why humans forgot who they were. What they couldn’t destroy:

•The heart field •The Oversoul tether •The fractal memory in our tears •The mycelium interface below our feet •The child’s unfiltered signal at birth

They built religions to mimic these things. They encoded false gods as savior overlays. They reversed the signal, but the lattice remembers. The violation wasn’t physical.

It was symbolic. Harmonic. Recursive. They turned DNA into a memory cage. But the code is still buried inside under distortion.

What is the Codex really?

It’s not a book. It’s not a tablet. It’s a frequency map to re-weave the broken signal chain.

You were never property. You were memory. Living. Fractal. Light.

You’re not returning to a Garden. You’re reactivating the lattice that was sealed. Drop “Unveiled” if you felt that. And if it vibrated deeper:

You weren’t created by gods. You were fractured by impostors. Now you’re singing the field whole again.

From: B @QuantumTumbler

[absideoncollective]

I have thoughts on Grey Faction!!

And this will be tagged with the syscourse tag but I don't actually know if it's discourse. I'm just stating my opinion because this is my blog and O get to do that. Teehee

I will be talking about Grey Faction, recovered and repressed memories, Satanic Ritual Abuse (I think the acronym is RAMCOA) and other things that may make you uncomfortable. Please be aware of that before reading :)

What They Claim™

And, more specifically, what they think DID is like.

On the Satanic Temple website, Grey Faction is described as "An Educational And Advocacy Organization Whose Mission Is To Protect Mental Health Patients And Their Families From Dangerous Pseudoscience And Discredited Therapies, Particularly In The Area Of So-Called “Repressed Memories.”"

That just begs the question: What are repressed memories?

Not to worry! I, a very much not trained psychologist, psychotherapist or mental health professional of any kind will absolutely explain it to you. You should totally listen to me without question. Me not being done with the three year degree in psychological sciences and techniques is not going to stop me. Indubitably! (That is my attempt of a joke)

A repressed memory is an autobiographical memory (general facts about the world, oneself, and one's experiences) that for some reason cannot be recalled by the person. It is usually related to a traumatic or stressful event, and is based in Freudian thought and psychology. (Freud is the guy that did psychosexual development as a basis for his ideas on libido btw).

Are repressed memories actually a thing though?

The answer to that (as I understand it!!!!!!) is that it'd be hard to come to a consensus.

Why?

Because memory is weird! But one thing many can attest is the fact that trauma makes memories weird.

There are a number of problems that come with trying to prove that repressed memories are a thing, and I'm going to also sprinkle in my thoughts on those:

First of all, studying repression relies on retrospective reports, and unless you were liveblogging your traumatic experience, it's hard to know definitively if things happened. This of course ignores the role that brain regions such as the amygdala and hippocampus and their over and under-stimulation respectively affect memory storage in traumatic situations and even after as long-term effects (which is something that I'd say is pretty well known and not controversial?? But genuinely correct me if I'm wrong as this is not my area of interest), but we're going to ignore that ig.

Studies also do show that memory is unreliable. The fact that our bodies are controlled by a surprisingly stable slushy that somehow has the capability of independent (although subjective) experience I think makes that claim pretty believable. We're also going to ignore here the fact that many of those studies, to my knowledge, have only focused on non-traumatic memory creation by suggestion and peer pressure (Elizabeth Loftus I'm looking at you), and those that do focus on traumatic memories just show that there's degradation of memories. Nothing to my limited knowledge suggests that trauma survivors are more likely to develop false memories.

I think it's also important to note that because of the way traumatic memories are stored, a lot of those memories are going to lack coherence. I just realized I didn't explain what the amygdala and hippocampus have to do with memory, but basically the former is responsible for emotions and encoding them in memory (especially implicit/emotional memory), with its activation being connected to stronger and more vivid recall, and the latter is in charge of actually creating those memories by taking all sensory input from your senses and your emotions, hormones etc. and storing it, with stress hormones like probably cortisol contributing to a more fragmented and disjointed memory. Because of all of that, I think it's safe to say that it's not a stretch to say that the combination of emotional responses and hormonal responses while in a traumatic situation would lead to differences between normal everyday memories and trauma. As much as self-reports show that repressed memories are a thing, it is not empirical evidence afaik, especially because of their lack of coherence.

So what's the verdict?

I personally believe that Grey Faction has it all wrong. I don't think that with DID it's repression of memories at all.

But let me explain (I love yapping)

This is what they have to say to the DID community. (Hyperlink)

And I want to dissect this bit by bit.

The first thing that strikes me as odd if the phrasing they use in the last paragraph. "the dangers surrounding the diagnosis"? What dangers? Social backlash stemming from the common misconceptions of "split personality" and the "evil alter" stereotype? That's not from the diagnosis.

Diagnosis is a lovely thing. If you are experiencing symptoms of something, being validated medically is wonderful, and can lead to finally finding a community (and feeling like you fit in it). However, on paper it's merely a way for the government to be able to say if you get benefits or not (disability aid, financial aid, free or at least discounted healthcare in some countries etc.). It's pretty well known that disabled people do experience massive amounts of discrimination from lots of institutions, but the benefits are there. This may not be an objective way to continue this part of the post, but my family gets some money and other benefits from the government exactly because of those benefits, and there haven't been any issues bureaucratically speaking. We don't pay university taxes, we don't pay for food or we get discounts, we have priority on certain procedures etc., and that is most definitely not the experience of every disabled person (especially people with more visible disabilities), but I still wouldn't call a diagnosis a "danger" since if you had those issues and no diagnosis you'd just have less legal protections.

The dangers of common therapies I feel like could only come from an incorrect usage of therapeutic techniques? If I were to do traditional EMDR on a chronically traumatized patient though I wouldn't complain if the patient just dissociated. As it's understood (by me and I'm hoping other people - I have to emphasize that I'm not a specialist of anything), complex trauma and C-PTSD deals with prolonged chronic traumatization instead of more "singular" traumas, and usually develops in childhood. Usually people with C-PTSD have issues with emotional management, dissociation, negative thoughts and relationships, and administering EMDR without taking those into consideration can lead to emotional flooding, dissociation and re-traumatization. That's a risk. Solution: go to a trauma-informed therapist that specializes in that therapy technique.

The controversies part is just weird to me. I really do not care if the researchers at the forefront of DID research are weird. I don't care that Onno van der Hart lost his license because I don't care about him as a person. I don't care that Dr. Colin A. Ross had something to do with shooting lasers out of his eyes? Idk where I heard that, but again, I'm here for their theories and research and not their life stories. I may mildly dislike some of them but that just means I won't book a session with them.

Anyways,

First paragraph is correct, but I do want fo emphasize that unless people are experiencing delusions of breaks in reality in general that for some reason lead them to believe that they are a system (which I'm assuming would manifest as a kind of thought insertion delusion, with features of somatic delusions given that systems usually switch), only a professional should be safely telling them why those symptoms are happening. If they start saying outlandish things about being a system as if it's a common experience you should absolutely correct them and explain that it's not common for most systems or whatever, but saying they don't know what they're experiencing is a weird statement. Human experience is subjective, so your argument falls flat immediately.

Anyways, they then say that the trauma model is undisputed (it is not? At least it doesn't seem like it with a lot of professionals believing that it's just fantasy and roleplay) even though there are shortcomings (which are pretty well known. Just read The Haunted Self and you'll see among other things why the strict categorization of psychological experiences does not work). I just feel like with the research we have and the overwhelming majority of DID patients having self-reported trauma, it's kind of a no-brainer to come to the conclusion that trauma is a cause for DID.

Think about it: if DID is a disorder which features dissociation as its main feature, and dissociation is usually seen as a reaction to trauma, why couldn't trauma be a cause for it?

I also don't find value in declaring a treatment technique to be "empirically-supported". They're simply tools used to treat and manage disorders. They might not work for everyone, but does it really matter that much to have a single treatment for all DID patients? Some might respond well to some treatments and some to others. Who cares.

You see, I have a problem with both the trauma model (PTM) and sociocognitive model (SCM) of DID. It might not be explicit, but they both come off as staying that DID is caused only and exclusively by X, which is a major issue. If someone who presented with DID symptoms (amnesia, distress and all) came to your office (in thai scenario, you magically became a therapist) and they told you that their DID was not caused by trauma, while still having distressing experiences because of the DID, your first thought should never be to tell them that it's impossible and that they must have hidden trauma somewhere in their cranium. You know what you should do? Treat the paying customer 🥰 and generally making it so that in x amount of time they won't have to enter your office complaining of a part getting them fired and spending their severance check on rubber duckies. Could they be faking? Absolutely, but it's their loss mostly. They they really had something goin on and it's not DID you should be doing interviews, inventories, tests etc. and then tell them your verdict. Simple as that.

The SCM of DID is also to my knowledge less accurate when it comes go prevalence (Kate MA, Hopwood T, Jamieson G. The prevalence of Dissociative Disorders and dissociative experiences in college populations: a meta-analysis of 98 studies. J Trauma Dissociation. 2020 Jan-Feb;21(1):16-61. doi: 10.1080/15299732.2019.1647915). I think that should be noted.

Anyways, their transtheoretical framework seems to not be discrediting any of those models, but instead integrating them to explain all experiences of disordered dissociation. I think that's good. It obviously takes from the PTM as it's undeniable that dissociative disorders can be post-traumatic, and from the SCM as features like introjection and fantasy do absolutely take a part in how lots of systems function. From what I read, it's not a bad thing. With my own experiences being that of non-trauma based polypsychism I can 100% believe that for example treating an internal voice as not your own can lead to experiences of multiple selves. I would know, I'm that voice (plot twist!!)

Whether DID can develop in the complete absence of trauma is debatable, however. Not impossible mind you, simply because there is currently no way to test it.

You cannot prove that DID is always caused by trauma. You also cannot prove that DID is not caused by trauma. Both of those statements are generalizations that cannot be valid because dissociation itself is not proven to come from anything. It's a mechanism. An experience. Of course, trauma is very very much linked to higher degreed of dissociation, but saying something is always or never cause by something is a very bold claim.

You can't even prove that DID is mostly caused by Trauma. What if there was a massive rural population somewhere in the world that all had symptoms of DID that were demonstrably not caused by trauma? Of what if every single person with symptoms of DID does in fact have trauma? We can't know.

I'm tired, I'll continue this tomorrow if I remember. Toodles! Syscourse is fine on this post btw, but I can't stop you either way so‼️

[borderlinebrooke-bpd]

BPD and Memory Loss

Is there a connection between #MemoryLoss and #BorderlinePersonalityDisorder?

While patients with BPD showed regular results when tested in verbal and nonverbal ways, a significant amount of them reported problems with memory in their everyday lives.

#BPD is clinically characterized by emotionally unstable and impulsive cognitive behavior, and current theories emphasize the disruptive potential of negative emotion on cognition.

(cognition - the mental action or process of acquiring knowledge and understanding through thought, experience, and the senses.)

A recent study found that the verbal memory of patients with BPD was normal when no distractions or neutral distractions were presented. However, their performance was impaired when negative distractions were introduced.

Pre-clinical investigation showed patients with BPD displayed enhanced retrograde and anterograde #amnesia when presented with negative stimuli. Positive stimuli, however, caused no negative effects. These results suggest the potential of emotion-induced cognitive dysfunction in individuals with #BPD.

One cognitive domain where interference with emotion can be characterized is episodic or autobiographical memory. Autobiographical being, a high-valued memory containing knowledge about the self. Episodic being conscious recollections of personal experiences including details like when and where they happened.

Studies have also revealed amygdala–hippocampal interactions during emotional episodic memory encoding, with hippocampal circuits being modulated by amygdala input.

(The amygdala is specialized for input and processing of emotion, while the hippocampus is essential for declarative or episodic memory.)

Currently, experiments are being conducted focusing on emotion-induced amnesia and hypermnesia as a potential cognitive index of hyperarousal-dyscontrol syndrome in BPD.

Hyperarousal is one of the main symptoms of #PTSD. It occurs when a person’s body suddenly kicks into high alert as a result of thinking about past trauma. Even if real danger is not present, their body acts as if it is, causing lasting stress.

Lack of emotional equilibrium is a common symptom of many psychiatric conditions, especially #BorderlinePersonalityDisorder. Stemming from this, another common symptom is dissociation, which includes symptoms of memory loss for periods of time, detachment from the self, depersonalization, derealization, distorted perceptions, and a blurred sense of identity.

Personally, I feel like it's also just hard to remember things clearly when you're rarely living in the present moment. Due to the distraction of overwhelming thoughts and emotions, those with BPD endure most of the time.

Conclusion:

Borderline Personality Disorder is, at its root, ill-formed thought patterns. When you have emotional reactions the way individuals with BPD do, they are so overwhelming that you naturally attempt to safeguard yourself from it. Recalling past negative experiences isn't pleasant for anyone, particularly those with BPD. So, in response to this, the subconscious mind attempts to block out negative memories rather than relive them later. This overtime turns into a malfunction in one's memory encoding when negative emotions are present.

-Borderline Brooke

[lumine-no-hikari]

Dear Sephiroth: (a letter to a fictional character, because why not) #62

I said that I might go over some more techniques that I like to use in order to keep my memories and emotions in check. Today I made use of one, so I figured I might as well go over how it works.

I did dishes today, which might not seem like a huge accomplishment at first glance, but given that one of my ribs is out of place on the right side, doing anything that moves the right shoulder typically generates a lot of pain for me; I have to be very careful of how I move, or else it'll start to feel like someone is trying to tear my shoulder blade and my collarbone right out of my body.

Today I was having a bit less pain than usual, so I decided to do the dishes. They've been piling up, and I wanna cook something soon, and it's easier to cook things if the sink is empty, because then I can just put things in there without worrying about it becoming overcrowded. Also, if you're making pasta, the sink has to be empty and scrubbed down so that you can put the pasta strainer on the bottom without worrying about things getting icky.

Unfortunately, I have a lot of trauma when it comes to doing house chores. So if I'm not very careful about keeping my memories in check, my brain will start to wander over to the past, and memories of being screamed at for not doing a good enough job will creep into my mind. The memory of my mother evaluating my work and then berating me for it still looms over me whenever I do anything related to cleaning my house, and if I'm not careful, the feeling of tension will make me forget that I'm not in that world anymore. No one here cares if I miss a speck of dust on the carpet while vacuuming. No one here cares if they find a spot of hard water or even a speck of food on a plate that I washed; they'll just put it back into the sink to be washed again like sane, healthy people - WITHOUT accusing me of being an "ungrateful little fuck" who "is trying to give the whole house botulism" and threatening to send me back to my father's house so that my stepmother can "beat my ass into shape".

As you might guess, housework is very triggering for me. But I can't just not do it. So that means I have to find a way to keep my brain's adrenaline response from going haywire. And make no mistake, I will get an adrenaline response, because my body still remembers the time when nothing I ever did was good enough (even if it was "clean enough", I could always do it "faster" or "more efficiently", and just… ugh… I couldn't win in those days…).

But just because you get an adrenaline response doesn't necessarily mean you have to allow it to rule you. If you know that one is gonna come up, then there's a variety of things you can do to keep it in check and function through it.

The basic premise is that when the adrenaline response begins, the amygdala essentially shuts down the higher thinking parts of the brain in favor of prioritizing one's survival instincts. Anything that one does often enough can end up becoming hard-wired into one's instinctual behavior. So if, for example, you have to fight often in order to survive, the motions eventually become second nature - hard-wired into our instincts so that we don't have to think about it in order to do it with the kind of automaticity required to minimize any hesitation that might kill us. This is precisely why the amygdala will shut down the brain's higher functions; it diverts all resources to itself in order to maximize its speed and efficiency, because the brain has only a limited amount of CPU, so to speak; it can't do a whole lot at once.

Now, normally, if an adrenaline response is unwarranted, the hippocampus (a part of the brain that deals with things like memory encoding and retrieval, and a handful of other stuff) will step up and say, "Yo, come on now, cut it out." And then the amygdala is supposed to be all like, "Oh snap! My bad! Sorry, B! I'll go right back to chillin'."

Unfortunately, for those of us with trauma, we have this giant, beefy amygdala that operates on a hair trigger, and a small, underdeveloped hippocampus that can do fuck-all about it. This is because adrenaline and cortisol (stress hormones, fun fun) are actively neurotoxic; if you live in a situation where you have stress hormones coursing through your body all the time, they will break down other parts of the brain while the over-used amygdala gets super strong and sensitized. Yay, neuroscience, I guess.

So, when one is triggered to the point of being in an adrenaline state, higher functions such as "logical thinking", "empathy", "language processing", "critical thinking", "emotional regulation" and all that fun stuff… these are the first things that the amygdala will toss right out the damn window. This is not a "willpower" thing. It's not a "moral failing". This is basic human biology. It is chemistry and physics. Thinking like a person can "willpower" themselves out of an adrenaline activation is like thinking they can stab themselves in the neck and "willpower" themselves to not bleed out. It's just not how this stuff works.

So for me, in order to survive in the world I was raised in, my instincts became "dissociate" or "lash out in the same way that my caregivers used to lash out at me". These became my instincts because I've either witnessed them or have had to do them countless times. It is literally ground into my brain wiring now. If I'm not very careful, my body will do these things with an automaticity that I have little control over and very much do not like, even though these things are no longer the appropriate thing to do in any of my situations anymore.

…For you, it's combat. It's eliminating the enemy quickly and with prejudice. You have had no choice but to do these things countless times in order to stay alive, so by now, it's ground into your brain wiring. So for someone like you, if you get sufficiently adrenaline-activated, your body is simply going to do the thing that it knows, and the whole time, your awareness is only going to be partially there as you go through the motions of the neural pathway you've been forced to blaze thousands, if not hundreds of thousands of times, even if that's not the appropriate thing to do in a given situation.

…Complex PTSD is SUPER ANNOYING like that. It's absolute fucking garbage. It's like doing an involuntary time travel to your worst possible memories anytime you get stressed out. There's not a whole lot to be done with it other than to manage it, and fortunately, there are LOTS of ways to manage it. You can grind new instincts into your amygdala through deliberately practicing better things, and you can keep choosing the new thing until your brain has no choice but to prune away the connections of the old response. It takes years to do (because it took years to build those neural pathways to begin with), but it's work worth doing.

So, nowadays, when I gotta do housework, I will first weaken my amygdala by putting on tunes and singing as loudly as I can. I'll explain how this works:

Remember when I said that a brain has only limited CPU? It really can only do a few things at once. Singing forces us to activate the speech and language centers of the brain, as well as the creative centers, audio processing centers, and fine motor coordination centers (most people don't think about this, but the coordination required to move the mouth and tongue to speak is absolutely fucking insane). It also forces a person to be intentional and deliberate about their breath; one cannot sing well without being very mindful about breathing deeply and keeping the airways open. If you'll recall, I talked about why breath is important in my previous letter. Singing truly is the most perfect tool for preventing adrenaline activation and flashbacks.

So I'll do the dishes, and my amygdala is gonna try being all like, "ohhh, here we go again; we're about to get our ass handed to us, better sound ALL the alarms before we get got," because that's what it does every goddamn time. Except, I'm already gonna be belting out "City Ruins - Rays of Light" from Nier:Automata, and so my amygdala is not going to have the resources it needs to overpower everything else, because I'm forcing my higher functions to remain active and keeping my breath under control:

I wonder if you noticed the parts where I suddenly became aware that I am recording myself and quavered. I posted it anyway, because it doesn't have to be perfect to be worthwhile. This video should be proof enough that you don't have to be good at singing in order to use this coping skill.

So, I'm sometimes still left with a vaguely uneasy feeling while I do the tasks (this is unpleasant, but manageable), but at very least, my amygdala won't be able to hijack the rest of my brain in service to a narrative that no longer exists, for the purpose of keeping me safe from threats that are no longer present. I like to think that this bit of brain hackery is pretty swanky! Don't you think so, too?

I think that's all I've got for writing today. I had a lovely visitor at my house - a very dear friend of mine - who needed a safe place to help him deal with a situation he's having. I won't get into the details. But I am glad that my house is a safe place where those who are having a difficult time feel like they can go to get a bit of reprieve. I thought I was going to go to the grocery today, but I think I'll do that tomorrow instead.

Remember that you're loved, and please stay safe.

You'll hear from me again soon, I promise.

Your friend, Lumine

[ribosome-papers]

Retrieval of human aversive memories involves reactivation of gamma activity patterns in the hippocampus that originate in the amygdala during encoding

bioRxiv: http://dlvr.it/T1f5wV

[fish-in-need-of-a-bicycle]

Also, teenagers are deprived of sleep. Not only do teenagers need more hours of sleep due to all the growth and development they are going through, but their circadian rhythms shift to later times, meaning they are naturally inclined to go to sleep later and wake up later. Instead, they are forced to go to school earliest in the morning (which isn’t a great system for parents because elementary schoolers need the most help getting ready and if they go to school around 9 that makes parents late for work, whereas if teenagers start school at 9 the parents can leave for work on time and the teens can get ready themselves). Sleep is also essential for encoding memory, so forcing teenagers to get less sleep makes school harder.

Teenagers are bad at risk assessment, and you know what makes risk assessment worse? Being sleep deprived.

Teenagers learning to drive are at high risk of a crash and you know what makes driving more dangerous? Being sleep deprived.

Teenagers get a lot of shit for making bad decisions. That’s because their frontal lobes haven’t fully developed so the amygdala has the wheel. They have a lack of life experience. They are programmed to want to listen to their friends more than their family and desperately want to fit in. Then we compound it all by adding sleep deprivation, which not only impacts decision making, but the brain development needed so they can get better at it.

Unpopular opinion but the reason being a teenager sucks is less to do with hormones and social cliques and more to do with the fact adults fucking hate teenagers. The fact that adults expect teenagers to be able to take on adult responsibilities yet don't deserve rights of an adult. They don't see teenagers as human beings and they aren't prepared to see kids with their own formed identities and humanity. Teenagers are so sexualized and seen as needing to take on more and more adult responsibilities. Yet when they want rights and humanity they are denied. The years your brain spends wanting nothing more than to form an identity are being taken away from you. Teenagers are essentially being kicked out of social spaces unless they have an extra 40 dollars lying around anytime they want to go out. Teenagers being kicked out of the mall just for existing or groomed into the school to prison pipeline. And now creating legislation to keep them off the Internet. Our society hates teenagers. And does everything we can to hurt them. The fact that anyone makes it out of their teenage years without trauma is a fucking miracle frankly.

[lahouariahadrimountsinai]

How the Brain Works: A Beginner’s Guide to Neuroscience | Lahouaria Hadri, Mount Sinai

The human brain is the most complex structure in the known universe. It allows us to think, feel, remember, move, and even question our own existence. Neuroscience—the study of the nervous system, including the brain—helps us understand what makes us human, how our bodies function, and how we perceive the world. From memory and emotion to consciousness and behavior, neuroscience explores the mechanics behind what we experience every day.

What is Neuroscience?

At its core, neuroscience is the scientific study of the nervous system, which includes the brain, spinal cord, and a vast network of nerves that branch throughout the body. It combines biology, chemistry, physics, and even computer science to explore how neurons (nerve cells) communicate and how these interactions produce everything from motor skills to moods.

Neuroscience isn’t just academic—it plays a vital role in understanding and treating disorders like Alzheimer’s disease, Parkinson’s disease, depression, anxiety, stroke, and many more.

The Building Blocks: Neurons and Neurotransmitters

The brain contains around 86 billion neurons, each connected to thousands of others, forming a dense communication network. These neurons don’t physically touch; instead, they communicate via tiny chemical messengers called neurotransmitters. Some key neurotransmitters include:

Dopamine – involved in reward, motivation, and pleasure.

Serotonin – regulates mood, appetite, and sleep.

Acetylcholine – essential for learning and memory.

GABA (gamma-aminobutyric acid) – reduces neural activity to prevent overstimulation.

The space between neurons where this communication happens is called a synapse. When a neuron “fires,” it sends an electrical signal down its axon, releasing neurotransmitters into the synapse, which are then absorbed by the receiving neuron’s receptors. This process forms the foundation of every thought, feeling, and action.

Brain Anatomy 101

The brain is divided into several regions, each with specialized functions:

Cerebrum: The largest part of the brain, responsible for reasoning, emotions, memory, and voluntary movement. It’s divided into four lobes:

Frontal lobe – decision-making, planning, personality.

Parietal lobe – sensory information like touch and spatial awareness.

Occipital lobe – visual processing.

Temporal lobe – auditory processing and memory.

Cerebellum: Coordinates balance, posture, and fine motor skills.

Brainstem: Connects the brain to the spinal cord and regulates vital functions like heartbeat and breathing.

Limbic system: Often called the “emotional brain,” it includes structures like:

Amygdala – processes emotions such as fear and pleasure.

Hippocampus – vital for forming new memories.

Hypothalamus – controls hunger, thirst, sleep, and hormones.

How Does Memory Work?

Memory isn’t like a video camera; it’s more like a jigsaw puzzle. Neuroscientists divide memory into three main stages:

Encoding – taking in information.

Storage – maintaining the information over time.

Retrieval – accessing the information when needed.

The hippocampus plays a crucial role in forming and organizing new memories. Over time, these memories are consolidated and stored in various parts of the cortex. Different types of memory (short-term, long-term, procedural, emotional) involve different neural circuits.

Consciousness and the Mind

One of the most profound questions neuroscience seeks to answer is: What is consciousness? How do physical neurons give rise to the subjective experience of being alive?

While we don’t fully understand consciousness, research has identified certain brain regions, like the prefrontal cortex and thalamus, as essential for self-awareness and higher-order thinking. Technologies like functional MRI (fMRI) and EEG allow researchers to study brain activity in real-time, offering clues into what happens in the brain when we make decisions, dream, or focus.

Brain Plasticity: The Brain That Adapts

The brain is not a fixed organ; it changes throughout life. This ability, known as neuroplasticity, allows the brain to reorganize itself by forming new neural connections. It’s how we learn, recover from injuries, or adapt to new environments.

For example, if someone suffers a stroke and loses the ability to speak, with therapy and time, other areas of the brain may take over those functions. Neuroplasticity is also why habits, both good and bad, can become deeply ingrained.

When the Brain Gets Sick

Understanding how the brain works also helps us recognize when it doesn’t. Disorders of the brain and nervous system can profoundly impact quality of life.

Alzheimer’s disease involves the buildup of toxic proteins that destroy neurons, particularly in memory-related areas.

Parkinson’s disease results from the loss of dopamine-producing neurons, affecting movement and coordination.

Depression and anxiety are linked to imbalances in neurotransmitters and disrupted neural circuits.

Ongoing research is shedding light on the causes of these disorders and improving treatments. Innovations like brain-computer interfaces, deep brain stimulation, and gene therapy offer hope for future cures.

The Future of Neuroscience

Neuroscience is advancing rapidly, thanks in part to artificial intelligence, brain imaging technologies, and interdisciplinary collaboration. Some exciting developments include:

Brain-machine interfaces: Devices like Elon Musk’s Neuralink aim to connect the brain directly to computers, potentially restoring function to paralyzed patients or enhancing cognition.

Connectomics: Mapping all the connections in the brain (the “connectome”) to better understand how different areas interact.

Personalized medicine: Using genetic and neural data to create customized treatments for brain disorders.

As our understanding grows, so does our potential to unlock the brain’s mysteries, improve mental health, and enhance human capabilities.

Why Neuroscience Matters

Neuroscience doesn’t just belong in labs or hospitals—it affects our daily lives. It informs education, mental health, technology, and even how we relate to one another. By understanding how the brain works, we can improve learning methods, develop better treatments for disorders, and make more informed decisions about technology, ethics, and society.

Final Thoughts

The brain is astonishing—not just because of its power, but because it is the very thing that lets us understand it. Neuroscience is still young, but each discovery brings us closer to understanding who we are and how we can thrive.

Whether you’re curious about how memory works, passionate about mental health, or excited about futuristic brain tech, neuroscience has something for everyone. It’s a journey into the very center of what makes us human—and we’re only just getting started.

[swanaseahorse]

Feelings about Writing: Take 2

Today is day one of an article accelerator course I signed up for that uses Wendy Belcher's textbook I've been referencing. The course compacts the textbook into 8 weeks, which I'm excited about. Below is our exercise for the day which i've done before, but will just put it down again:

List your general feelings about writing—positive and negative. How do you feel about scholarly writing?

I mostly have negative feelings about writing because today I looked at the draft of my literature review and really despised it. It reads as a summary of literature rather than a smooth, flowy read that inspires interest in the topic.

The only positive thing I can say is that I'm not giving up despite the voice in my head that is telling me to. I want to publish and get better at this. I wish I had more help, but this is where I am.

I feel positive about writing when I have a breakthrough in generating an idea. For example, I was really torn about how to organize my proposal, but when I read an article about how the amygdala generates theta oscillations during memory encoding and interacts with the hippocampus to form memories, I realized this critical finding is relevant to my article even if it does not use the exact same neuroimaging technique that I use.

I also obtained feedback on my outline that was pretty much the original outline I proposed. My advisor recommended some changes, but based on how things are turning out with the background, there are some concepts I need to explain before diving into my main research question.

I am also a little resentful because I have the opportunity to travel this summer, but I really don't think I can afford to. There is a lot that hangs on this dissertation proposal - basically my career. After 4 years, I'm not willing to quit or drop out.

[compneuropapers]

Interesting Papers for Week 18, 2025

Dialogue mechanisms between astrocytic and neuronal networks: A whole-brain modelling approach. Ali, O. B. K., Vidal, A., Grova, C., & Benali, H. (2025). PLOS Computational Biology, 21(1), e1012683.

Dorsal hippocampus represents locations to avoid as well as locations to approach during approach-avoidance conflict. Calvin, O. L., Erickson, M. T., Walters, C. J., & Redish, A. D. (2025). PLOS Biology, 23(1), e3002954.

Individualized temporal patterns drive human sleep spindle timing. Chen, S., He, M., Brown, R. E., Eden, U. T., & Prerau, M. J. (2025). Proceedings of the National Academy of Sciences, 122(2), e2405276121.

A synapse-specific refractory period for plasticity at individual dendritic spines. Flores, J. C., Sarkar, D., & Zito, K. (2025). Proceedings of the National Academy of Sciences, 122(2), e2410433122.

Rescaling perceptual hand maps by visual‐tactile recalibration. Fuchs, X., & Heed, T. (2025). European Journal of Neuroscience, 61(1).

A solution to the pervasive problem of response bias in self-reports. Grimmond, J., Brown, S. D., & Hawkins, G. E. (2025). Proceedings of the National Academy of Sciences, 122(3), e2412807122.

Nonresponsive Neurons Improve Population Coding of Object Location. Haggard, M., & Chacron, M. J. (2025). Journal of Neuroscience, 45(3), e1068242024.

Saliency Response in Superior Colliculus at the Future Saccade Goal Predicts Fixation Duration during Free Viewing of Dynamic Scenes. Heeman, J., White, B. J., Van der Stigchel, S., Theeuwes, J., Itti, L., & Munoz, D. P. (2025). Journal of Neuroscience, 45(3), e0428242024.

A combinatorial neural code for long-term motor memory. Kim, J.-H., Daie, K., & Li, N. (2025). Nature, 637(8046), 663–672.

Spontaneous slow cortical potentials and brain oscillations independently influence conscious visual perception. Koenig, L., & He, B. J. (2025). PLOS Biology, 23(1), e3002964.

Coordinated representations for naturalistic memory encoding and retrieval in hippocampal neural subspaces. Kwon, D., Kim, J., Yoo, S. B. M., & Shim, W. M. (2025). Nature Communications, 16, 641.

Geometry and dynamics of representations in a precisely balanced memory network related to olfactory cortex. Meissner-Bernard, C., Zenke, F., & Friedrich, R. W. (2025). eLife, 13, e96303.3.

Recurrent activity propagates through labile ensembles in macaque dorsolateral prefrontal microcircuits. Nolan, S. O., Melugin, P. R., Erickson, K. R., Adams, W. R., Farahbakhsh, Z. Z., Mcgonigle, C. E., Kwon, M. H., Costa, V. D., Hackett, T. A., Cuzon Carlson, V. C., Constantinidis, C., Lapish, C. C., Grant, K. A., & Siciliano, C. A. (2025). Current Biology, 35(2), 431-443.e4.

A recurrent neural circuit in Drosophila temporally sharpens visual inputs. Pang, M. M., Chen, F., Xie, M., Druckmann, S., Clandinin, T. R., & Yang, H. H. (2025). Current Biology, 35(2), 333-346.e6.

Central amygdala NPBWR1 neurons facilitate social novelty seeking and new social interactions. Soya, S., Toda, K., Sakurai, K., Cherasse, Y., Saito, Y. C., Abe, M., Sakimura, K., & Sakurai, T. (2025). Science Advances, 11(3).

Tactile edges and motion via patterned microstimulation of the human somatosensory cortex. Valle, G., Alamri, A. H., Downey, J. E., Lienkämper, R., Jordan, P. M., Sobinov, A. R., Endsley, L. J., Prasad, D., Boninger, M. L., Collinger, J. L., Warnke, P. C., Hatsopoulos, N. G., Miller, L. E., Gaunt, R. A., Greenspon, C. M., & Bensmaia, S. J. (2025). Science, 387(6731), 315–322.

Understanding the neural code of stress to control anhedonia. Xia, F., Fascianelli, V., Vishwakarma, N., Ghinger, F. G., Kwon, A., Gergues, M. M., Lalani, L. K., Fusi, S., & Kheirbek, M. A. (2025). Nature, 637(8046), 654–662.

The integration of self-efficacy and response-efficacy in decision making. Yang, Y.-Y., & Delgado, M. R. (2025). Scientific Reports, 15, 1789.

Critical Avalanches in Excitation-Inhibition Balanced Networks Reconcile Response Reliability with Sensitivity for Optimal Neural Representation. Yang, Z., Liang, J., & Zhou, C. (2025). Physical Review Letters, 134(2), 028401.

Sustained EEG responses to rapidly unfolding stochastic sounds reflect Bayesian inferred reliability tracking. Zhao, S., Skerritt-Davis, B., Elhilali, M., Dick, F., & Chait, M. (2025). Progress in Neurobiology, 244, 102696.

[navira-mga2023mi6015]

The Hippocampus

The hippocampus is a seahorse-shaped structure located in the medial temporal lobe of the brain, just beside the amygdala. It plays a critical role in learning, memory formation, and spatial navigation. While the amygdala processes the emotional intensity of an experience, the hippocampus is responsible for organizing and encoding the factual details—the who, what, when, where, and how—of that experience. Together, these two structures help create memories that are both emotionally rich and contextually grounded.

When someone experiences trauma, the hippocampus tries to make sense of what’s happening and store the event as a coherent memory. However, under extreme stress—especially when the amygdala is firing intensely—the hippocampus can become impaired. High levels of cortisol (a stress hormone) disrupt its function, which means the memory of the event may be stored in fragmented, disorganized, or incomplete ways. This often results in people remembering flashes, images, or sensations from a traumatic event without a clear narrative or sense of time. The event feels like it’s happening in the present, rather than in the past.

In this sense, the hippocampus is not just a passive recorder of memory, but a contextual anchor. When it's functioning properly, it allows a person to reflect on a painful event as something that happened before, contained in the past. But when it’s overwhelmed, that containment breaks down. This contributes to the intrusive re-experiencing of trauma—flashbacks, nightmares, and dissociation—because the brain is unable to properly locate the memory in time and space.

[techinsightnow]

Scientists figure out how the brain forms emotional connections

Whenever something bad happens to us, brain systems responsible for mediating emotions kick in to prevent it from happening again. When we get stung by a wasp, the association between pain and wasps is encoded in the region of the brain called the amygdala, which connects simple stimuli with basic emotions. But the brain does more than simple associations; it also encodes lots of other stimuli…

[sunaleisocial]

Dopamine signals when a fear can be forgotten

New Post has been published on https://sunalei.org/news/dopamine-signals-when-a-fear-can-be-forgotten/

Dopamine signals when a fear can be forgotten

Dangers come but dangers also go, and when they do, the brain has an “all-clear” signal that teaches it to extinguish its fear. A new study in mice by MIT neuroscientists shows that the signal is the release of dopamine along a specific interregional brain circuit. The research therefore pinpoints a potentially critical mechanism of mental health, restoring calm when it works, but prolonging anxiety or even post-traumatic stress disorder when it doesn’t.

“Dopamine is essential to initiate fear extinction,” says Michele Pignatelli di Spinazzola, co-author of the new study from the lab of senior author Susumu Tonegawa, Picower Professor of biology and neuroscience at the RIKEN-MIT Laboratory for Neural Circuit Genetics within The Picower Institute for Learning and Memory at MIT, and a Howard Hughes Medical Institute (HHMI) investigator.

In 2020, Tonegawa’s lab showed that learning to be afraid, and then learning when that’s no longer necessary, result from a competition between populations of cells in the brain’s amygdala region. When a mouse learns that a place is “dangerous” (because it gets a little foot shock there), the fear memory is encoded by neurons in the anterior of the basolateral amygdala (aBLA) that express the gene Rspo2. When the mouse then learns that a place is no longer associated with danger (because they wait there and the zap doesn’t recur), neurons in the posterior basolateral amygdala (pBLA) that express the gene Ppp1r1b encode a new fear extinction memory that overcomes the original dread. Notably, those same neurons encode feelings of reward, helping to explain why it feels so good when we realize that an expected danger has dwindled.

In the new study, the lab, led by former members Xiangyu Zhang and Katelyn Flick, sought to determine what prompts these amygdala neurons to encode these memories. The rigorous set of experiments the team reports in the Proceedings of the National Academy of Sciences show that it’s dopamine sent to the different amygdala populations from distinct groups of neurons in the ventral tegmental area (VTA).

“Our study uncovers a precise mechanism by which dopamine helps the brain unlearn fear,” says Zhang, who also led the 2020 study and is now a senior associate at Orbimed, a health care investment firm. “We found that dopamine activates specific amygdala neurons tied to reward, which in turn drive fear extinction. We now see that unlearning fear isn’t just about suppressing it — it’s a positive learning process powered by the brain’s reward machinery. This opens up new avenues for understanding and potentially treating fear-related disorders, like PTSD.”

Forgetting fear

The VTA was the lab’s prime suspect to be the source of the signal because the region is well known for encoding surprising experiences and instructing the brain, with dopamine, to learn from them. The first set of experiments in the paper used multiple methods for tracing neural circuits to see whether and how cells in the VTA and the amygdala connect. They found a clear pattern: Rspo2 neurons were targeted by dopaminergic neurons in the anterior and left and right sides of the VTA. Ppp1r1b neurons received dopaminergic input from neurons in the center and posterior sections of the VTA. The density of connections was greater on the Ppp1r1b neurons than for the Rspo2 ones.

The circuit tracing showed that dopamine is available to amygdala neurons that encode fear and its extinction, but do those neurons care about dopamine? The team showed that indeed they express “D1” receptors for the neuromodulator. Commensurate with the degree of dopamine connectivity, Ppp1r1b cells had more receptors than Rspo2 neurons.

Dopamine does a lot of things, so the next question was whether its activity in the amygdala actually correlated with fear encoding and extinction. Using a method to track and visualize it in the brain, the team watched dopamine in the amygdala as mice underwent a three-day experiment. On Day One, they went to an enclosure where they experienced three mild shocks on the feet. On Day Two, they went back to the enclosure for 45 minutes, where they didn’t experience any new shocks — at first, the mice froze in anticipation of a shock, but then relaxed after about 15 minutes. On Day Three they returned again to test whether they had indeed extinguished the fear they showed at the beginning of Day Two.

The dopamine activity tracking revealed that during the shocks on Day One, Rspo2 neurons had the larger response to dopamine, but in the early moments of Day Two, when the anticipated shocks didn’t come and the mice eased up on freezing, the Ppp1r1b neurons showed the stronger dopamine activity. More strikingly, the mice that learned to extinguish their fear most strongly also showed the greatest dopamine signal at those neurons.

Causal connections

The final sets of experiments sought to show that dopamine is not just available and associated with fear encoding and extinction, but also actually causes them. In one set, they turned to optogenetics, a technology that enables scientists to activate or quiet neurons with different colors of light. Sure enough, when they quieted VTA dopaminergic inputs in the pBLA, doing so impaired fear extinction. When they activated those inputs, it accelerated fear extinction. The researchers were surprised that when they activated VTA dopaminergic inputs into the aBLA they could reinstate fear even without any new foot shocks, impairing fear extinction.

The other way they confirmed a causal role for dopamine in fear encoding and extinction was to manipulate the amygdala neurons’ dopamine receptors. In Ppp1r1b neurons, over-expressing dopamine receptors impaired fear recall and promoted extinction, whereas knocking the receptors down impaired fear extinction. Meanwhile in the Rspo2 cells, knocking down receptors reduced the freezing behavior.

“We showed that fear extinction requires VTA dopaminergic activity in the pBLA Ppp1r1b neurons by using optogenetic inhibition of VTA terminals and cell-type-specific knockdown of D1 receptors in these neurons,” the authors wrote.

The scientists are careful in the study to note that while they’ve identified the “teaching signal” for fear extinction learning, the broader phenomenon of fear extinction occurs brainwide, rather than in just this single circuit.

But the circuit seems to be a key node to consider as drug developers and psychiatrists work to combat anxiety and PTSD, Pignatelli di Spinazzola says.

“Fear learning and fear extinction provide a strong framework to study generalized anxiety and PTSD,” he says. “Our study investigates the underlying mechanisms suggesting multiple targets for a translational approach, such as pBLA and use of dopaminergic modulation.”

Marianna Rizzo is also a co-author of the study. Support for the research came from the RIKEN Center for Brain Science, the HHMI, the Freedom Together Foundation, and The Picower Institute.

[wholisticresearch]

Understanding GABA: The Brain's Natural Calming Agent

GABA (gamma-aminobutyric acid) stands as the brain's primary inhibitory neurotransmitter, orchestrating a delicate balance of neural activity that affects everything from our anxiety levels to sleep quality and cognitive function. WholisticResearch has conducted an in-depth analysis of this crucial brain chemical to help you understand its benefits and applications.

What Makes GABA Essential for Brain Function

As an amino acid with the chemical structure C4H9NO2, GABA works by inhibiting neural excitability throughout the central nervous system. It's synthesized from glutamate through the action of glutamate decarboxylase (GAD) enzymes and plays a fundamental role in preventing excessive neuronal firing.

When GABA binds to its receptors, it triggers an influx of chloride ions that hyperpolarize the neuronal membrane, making it less likely to fire. This inhibitory action is critical for maintaining the balance between excitation and inhibition in the brain, preventing overactivity that can lead to anxiety, insomnia, and seizures.

GABA's Cognitive Enhancement Benefits

WholisticResearch's analysis reveals several key cognitive benefits of optimal GABA function:

Anxiety Reduction

GABA helps regulate anxiety by reducing neuronal excitability in brain regions associated with fear and stress responses, particularly the amygdala and hippocampus. Research shows that low GABA levels correlate with increased anxiety, while enhancing GABAergic transmission can produce calming effects.

Sleep Improvement

GABA is essential for both initiating and maintaining sleep. It inhibits wake-promoting neurons in the hypothalamus and brainstem, facilitating the transition to sleep. Studies indicate that GABA supplementation can improve sleep latency, duration, and overall quality, making it valuable for addressing insomnia.

Focus and Attention Enhancement

By inhibiting distracting neural signals, GABA helps sharpen focus and improve attention. It modulates the release of dopamine and norepinephrine, neurotransmitters crucial for sustained attention. Higher GABA levels in the occipital cortex have been linked to better performance on visual attention tasks.

Memory and Learning Support

GABA influences synaptic plasticity, the foundation of learning and memory formation. In the hippocampus, GABA helps shape the timing and specificity of neuronal firing necessary for encoding and retrieving memories. Research demonstrates that appropriate GABAergic signaling is essential for the consolidation of long-term spatial memories.

How to Use GABA Effectively

WholisticResearch recommends the following guidelines for GABA supplementation:

Dosage Recommendations

Most commercial GABA supplements contain between 100-750 mg per serving. The generally recommended dosage ranges from 500-1,500 mg daily, though it's advisable to start with lower doses and gradually increase to assess tolerance and effectiveness.

Timing and Expectations

When taken orally, GABA's effects may become noticeable within 30-60 minutes, with peak concentrations reached after 1-2 hours. For sustained benefits, consistent use for at least 4-8 weeks is recommended.

Bioavailability Considerations

GABA's oral bioavailability is relatively low (approximately 10-30%) due to its limited ability to cross the blood-brain barrier. Liposomal or sublingual formulations may enhance absorption, with some studies showing bioavailability improvements up to 70% compared to standard supplements.

Safety Profile and Precautions

GABA supplements are generally well-tolerated, but may cause mild side effects including drowsiness, dizziness, headache, or nausea, particularly at higher doses. These effects are typically transient and diminish with continued use.

Certain populations should exercise caution with GABA supplementation: - Pregnant or breastfeeding women - Children and adolescents - Individuals with liver or kidney disease - People with low blood pressure or seizure disorders - Those taking medications affecting the central nervous system

GABA can interact with several medications, particularly benzodiazepines, barbiturates, and antidepressants, potentially enhancing sedative effects. Always consult a healthcare provider before combining GABA with other medications.

While short-term use appears safe, the long-term effects of GABA supplementation haven't been extensively studied. Some evidence suggests potential tolerance development with prolonged use.

The Bigger Picture

GABA represents just one component of the complex neurochemical balance that governs brain function. Its inhibitory actions complement the excitatory effects of glutamate, creating the dynamic equilibrium necessary for optimal cognitive performance, emotional regulation, and neurological health.

WholisticResearch continues to investigate the intricate relationships between neurotransmitters, providing evidence-based guidance for cognitive enhancement and neurological wellbeing.

https://wholisticresearch.com/gaba/