#dopamine — Public Fediverse posts
Live and recent posts from across the Fediverse tagged #dopamine, aggregated by home.social.
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https://www.youtube.com/watch?v=w1pwBsaoY0Y
They are leveraging your #dopamine to turn you into their cog in their machine.
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Eh, you're keeping an industry afloat!
The #Neuroscience of Why You Can’t Stop Buying #Books You Don’t Have Time to #Read https://www.inc.com/jessica-stillman/the-neuroscience-of-why-you-cant-stop-buying-books-you-dont-have-time-to-read/91377269
#tsundoku #curiosity #dopamine #anticipation #amreading #collectors
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DATE: August 20, 2026 at 11:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Scientists discover an epigenetic mechanism that links childhood trauma to adult stress sensitivity
Experiencing trauma during early development suggests a lasting alteration in how brain cells package their DNA, leaving individuals more vulnerable to stress later in life. A recent study published in the journal Neuron indicates that early-life adversity increases a specific enzyme that keeps DNA loosely coiled in a key brain region, making the brain hyper-reactive to future stressors. Preventing this molecular change protected mice from developing heightened stress sensitivity in adulthood.
Childhood trauma and severe early-life stress are known risk factors for anxiety, depression, and other mood disorders in adulthood. The authors of the current study aimed to understand the physical mechanisms that allow trauma during early development to alter the brain permanently.
“Millions of children experience stress while growing up,” explained Catherine Jensen Peña, an assistant professor at the Princeton Neuroscience Institute. “We’ve known for decades that the more stress a child encounters, the greater the risk for additional stress later in life to precipitate anxiety, depression, or addiction. But we’ve known very little about the biology of that latent vulnerability. Ultimately, we hope this research can help point to new treatments to ease this stress sensitivity.”
To investigate this, the scientists focused on the ventral tegmental area, a brain region rich in dopamine-producing neurons that processes rewards and adversity. Within these dopamine cells, the scientists examined the epigenome. The epigenome consists of molecular tags that attach to DNA and determine whether specific genes are turned on or off.
Inside the nucleus, DNA is tightly wound around proteins called histones, resembling a coiled spring. When the DNA coil is compressed, the genes are hidden and turned off, but when chemical tags cause the coil to stretch and open, the genes become accessible and can be easily activated by environmental triggers.
“The effects of childhood adversity may not be immediately obvious, and sometimes manifests much later in life as exaggerated sensitivity to new stress encounters,” Peña told PsyPost. “We found one biological mechanism for this latent sensitivity at the epigenetic interface of nature and nurture.”
To observe how early-life stress alters these molecular tags, the researchers first used an analytical technique called mass spectrometry on brain tissue. They compared samples from 18 adult male mice, half of which experienced standard rearing and half of which were exposed to early-life stress. The stress condition involved separating the pups from their mothers for a few hours a day and reducing their nesting material between their tenth and seventeenth days of life.
The analysis indicated that early-life stress persistently altered the proportions of multiple histone modifications in the ventral tegmental area. Specifically, the stressed mice showed increased levels of 14 different modifications that are generally associated with a permissive, open DNA state. The researchers noted a large statistical effect size for a specific chemical tag called H3K4me1, which they then validated using protein analysis in a separate cohort of 27 male and female mice.
The scientists next sought to identify the enzyme responsible for adding this H3K4me1 tag to the histones. They analyzed RNA sequencing data from eight male mice and conducted genetic expression tests on a new cohort of 21 male and female mice, comparing standard-reared and stress-reared groups. The early-life stress condition increased the expression of Setd7, the gene that produces the enzyme responsible for placing the H3K4me1 tag, leaving the DNA structure stretched open.
To test if increasing this enzyme mimics the effects of early-life stress, the researchers used viral vectors to artificially overexpress Setd7 in the ventral tegmental area of juvenile mice. This approach acted as a form of genetic manipulation to introduce the enzyme, but it did not dictate exactly which genes the enzyme targeted.
“Increasing SETD7 was a fairly broad, non-specific tool (we didn’t have control over where the enzyme was depositing H3K4me1 around the genome) so it was a bit of a long-shot that it worked to mimic early-life stress,” Peña told PsyPost. “We don’t yet know if there is specificity in where early-life stress acts throughout the genome, or if the broad scatter-shot approach is the point.”
They compared this genetically altered group to a control group that received a neutral viral vector. Once the mice reached adulthood, they were exposed to a short social defeat stress protocol, and the researchers then sequenced the RNA from the brain tissue of 13 mice to observe gene activity.
In the control mice, the adult stressor mostly suppressed gene activity, decreasing the expression of 99 genes and increasing 39. In the mice with artificially boosted Setd7, the opposite occurred. The adult stressor increased the expression of 48 genes and decreased only three, providing evidence that the open DNA structure primed the cells for a hyper-active genetic response to stress.
The researchers also measured the electrical activity of the dopamine neurons. They artificially increased Setd7 in another group of juvenile mice, and during adulthood, these mice experienced three days of unpredictable stressors, such as tail suspension and mild foot shocks. The scientists then used microscopic electrodes to record the electrical firing of dopamine neurons in about 36 mice across the different experimental and control groups.
Increasing Setd7 did not change the baseline electrical activity of the dopamine cells in unstressed mice. Following the adult stress protocol, however, the dopamine neurons in the Setd7-boosted mice fired much more rapidly in response to stimulation and showed a higher baseline electrical current compared to the control mice. This indicates that the epigenetic changes specifically lowered the cells’ tolerance to future stress, rather than simply raising their baseline activity.
To observe how this hyper-reactivity affects behavior, the researchers tested 28 mice, split evenly by sex. Half received the Setd7 boost as juveniles, and half received a control vector. As adults, the mice underwent a social interaction test and an open field exploration test before and after experiencing social defeat stress.
The brief adult stressor did not strongly affect the behavior of the control mice. For the Setd7-boosted mice, the adult stressor reduced their social interaction time and decreased the time they spent exploring the center of an open field. This behavioral shift suggests that artificially opening the DNA structure is sufficient to make mice more susceptible to adult stress.
Finally, the researchers tested whether blocking this enzyme could prevent stress sensitivity. They used a customized viral vector to reduce Setd7 levels in the ventral tegmental area of juvenile mice that had actually experienced early-life stress. They tested the behavior of roughly 50 mice, including standard-reared and stress-reared groups with and without the genetic reduction, before and after adult stress.
Mice exposed to early-life stress typically showed reduced social interaction and more anxious behavior following adult stress. Reducing the Setd7 enzyme prevented these behavioral changes. The mice with lowered Setd7 levels remained social and exploratory after the adult stressor, mirroring the resilience of mice that never experienced early-life trauma.
The research involves certain limitations regarding the precision of the genetic tools used. The viral vector used to increase the Setd7 enzyme operated across all cell types in the targeted brain region, not just dopamine neurons. This broad application means the resulting behavioral changes could partially stem from alterations in neighboring non-dopamine cells. Future studies will need to use more advanced gene-editing techniques to target epigenetic modifications to specific cell types and precise locations on the DNA coil.
The viral vectors allowed the researchers to successfully reduce Setd7 and prevent stress sensitivity in mice, but translating this to human medical care presents immense hurdles. “We used a form of gene therapy to ameliorate the effects of early-life stress in this study, but we are far from using that safely and ethically in humans, especially in a preventative manner,” Peña explained. “Instead, we might explore whether we can harness the extra sensitivity early-life stress bestows, but in positive contexts.”
This future direction aligns with the fact that the current experiments focused only on aversive stressors. It remains unknown if this epigenetic priming mechanism might also make the brain more sensitive to positive, enriching experiences in adulthood.
The study, “Early-life stress alters H3K4me1 in VTA to prime stress sensitivity,” was authored by Hye Ji J. Kim, Luke T. Geiger, Julie-Anne Balouek, Lisa Z. Fang, Mason R. Barrett, Jeremy M. Thompson, Lorna A. Farrelly, Travis Hage, Rixing Lin, Andy S. Chen, Megan Tang, Hao Huang, Anna Buretta, Agatha Chan, Shannon N. Bennett, Benjamin A. Garcia, Ian Maze, Meaghan C. Creed, and Catherine Jensen Peña.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #EarlyLifeStress #Epigenetics #H3K4me1 #SETD7 #VTA #Dopamine #StressSensitivity #Neuroscience #TraumaAndBrain #NeuronStudy
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The Shocking Truth About Sugar & Energy 😮
#sugar #energy #dopamine #healthtips #nutrition #mitochondria #sugarfacts #wellness #healthychoices #sciencefacts #healthyliving #foodscience #shorts #shortsvideo -
A new ADHD drug targets three brain chemicals instead of two. Here’s what that means
#Health #Centanafadine #ADHD #ADHDTreatment #Simtriyo #MentalHealth #Neuroscience #Dopamine #Stimulants #Healthcare #Medicine
https://the-14.com/a-new-adhd-drug-targets-three-brain-chemicals-instead-of-two-heres-what-that-means/ -
A case-control study of 24 adults with long COVID and age-matched controls found that the long COVID patients had fewer neurons in the brain's striatum region that signal with dopamine. This deficit may be associated with reductions in movement and motivation.
Summary: https://www.sciencealert.com/long-covid-linked-to-lasting-damage-in-the-brains-dopamine-system
Original paper: https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(26)00222-7/fulltext
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Dopamine 3 permet désormais de jailbreaker iOS 26 http://dlvr.it/TTxPGv #Dopamine #Jailbreak
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¡Por fin!
Tras 326 días, Dopamine 3.0 trae el primer jailbreak para iOS 26 (A12/A13) y amplía soporte a iOS 16.5.1-17.3.1.
¡La comunidad celebra!
#Jailbreak #Dopaminehttps://locosdemanzana.es/2026/08/08/ios-26-ya-tiene-jailbreak-gracias-a-dopamine/
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Doing all the things…
...that I think I "need" to keep doing... Following "the rules", doing the same thing over and over, and never thinking it really matters... 😔 And then wondering why I keep doing it... Every time I think I'm done, it all "just" starts over again. 😢 And I know that this is the same for everyone. But, some moments, I just struggle so much with it, because I feel so exhausted, that I don't want to do it anymore... 😔 Why should I try to clean, when it will get dirty again? Why should I try to become more healthy? I'll mess up again, and get all obese and out-of-shape again... Why do I want to get new things, when I can't seem to enjoy things I have? 😢 […]https://cynnisblog.wordpress.com/2026/08/07/doing-all-the-things/
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You've never met yourself at your current age, but 1 year sober. You can be so much better... but you need to reclaim yourself first. It's like slowly becoming awake, snapping out of constant, generational narcosis. 3/3
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Because I see my life after the addiction, and I am yet to take it from there. But every time I go through this cycle, my life slowly begins to improve. And the connection with whatever's out there (God, cosmic intelligence, The Universe) becomes stonger and clearer. I'm not religious, btw. And I begin to need less, which honestly feels like "freedom." If you're on the fence about quitting something or even becoming "straight edge," go for it. 2/3
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It's an uncomfortable truth that people would rather ruin their lives than face the truth of their life (which at this time will be uncomfortable). That seems the paradox of addiction. And I'm not talking "heroin." Weed, video games, netflix, PMO, recreational eating, and so on. Every time I quit an addiction, it's as if I peel-off a layer and I see my life more clearly. And at this point in time, it's usually a bit disappointing to see. 1/3
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I just read an old comment of mine, under the YT video "Does Weed Steal Your Soul?" I had completely forgotten about it. Surprisingly candid. And on addiction, of course. Thought I'd repost here... 🧵
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Sleep Apnea's Hidden Path to Memory Loss Runs Through Dopamine
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@jwildeboer I am experiencing this very well recently, I opened an account on #Twitter recently and feels much more difficult than #mastodon.
Everything seems designed to pay, if you don't pay no one is going read you. Free accounts are only for followers addicted to #dopamine.
Don't understand why people still there. Interesting people, but cannot call it as #socialnetwork.
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So, a person who goes chasing dopamine -- somebody like me who has ADHD, for instance -- is a miner for dopamine. A dopaminer.
✳️✳️✳️A dopa-MINER.✳️✳️✳️
#dopamine
#dopaminer
#Dopaminecraft
#ADHD
#DAVE
#DopamineAttentionVariabiltyExecutiveDysfunction -
https://www.youtube.com/watch?v=8xWpbS8V6BU
A lucidly informing illumination of the #dopamine hijacking effect of #dooomscrolling. All effects are nailed.
This is an international epidemic matter.
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The fascinating science of pleasure goes way beyond dopamine
https://psyche.co/ideas/the-fascinating-science-of-pleasure-goes-way-beyond-dopamine
Dean Burnett writes for Psyche Magazine about a particular bugbear of his; the mainstream misunderstanding of dopamine and its link to pleasure
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Not that specifically, but, eh, I just go wherever the #dopamine leads me 😆
I've never been addicted to, or even tried "recreational pharmaceuticals," but I'm waaaay too dependent on that stupid little molecule 😅💦
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Ah, #capitalism at its finest: creating a buffet of #dopamine while the European Commission plays whac-a-mole with #ethics violations. 😅 #Meta raises its glass to #addiction as a key performance indicator! 🍾📈
https://kasperjunge.com/blog/capitalism-gone-wrong/ #performanceindicator #HackerNews #ngated
