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Your Heart’s Secret: It Has Its Own Nervous System

Summary: New research reveals the heart has its own complex nervous system, or “mini-brain,” capable of regulating the heartbeat independently of the brain. Conducted on zebrafish, the study identified specialized neurons within the heart, including some with pacemaker properties, challenging traditional views of heartbeat control.

This discovery provides new insights into heart diseases and potential treatments for conditions like arrhythmias. Researchers aim to explore how this cardiac nervous system interacts with the brain during stress, exercise, or disease to identify novel therapeutic targets.

The Seeds of Schizophrenia May Be Planted in The Earliest Moments of Life

There’s a window of time in our lives we’ve all passed through yet still know so little about: early gestation. Researchers have found a pair of genetic deletions associated with schizophrenia that likely occur in that formative period.

The discovery comes from a team of researchers led by Harvard Medical School clinician-scientist Eduardo Maury, who combed through genetic data from blood samples of nearly 25,000 people with or without schizophrenia.

While the two genetic alterations need further validation, the findings strengthen an emerging idea that the seeds of schizophrenia aren’t always inherited, yet still may be acquired long before someone meets the world.

The Cause of Alzheimer’s Might Be Coming From Inside Your Mouth

In recent years, a growing number of scientific studies have backed an alarming hypothesis: Alzheimer’s disease isn’t just a disease, it’s an infection.

While the exact mechanisms of this infection are something researchers are still trying to isolate, numerous studies suggest the deadly spread of Alzheimer’s goes way beyond what we used to think.

One such study, published in 2019, suggested what could be one of the most definitive leads yet for a bacterial culprit behind Alzheimer’s, and it comes from a somewhat unexpected quarter: gum disease.

A brain-controlled exoskeleton has let a paralyzed man walk in the lab

The news: A paralyzed man has walked again thanks to a brain-controlled exoskeleton suit. Within the safety of a lab setting, he was also able to control the suit’s arms and hands, using two sensors on his brain. The patient was a man from Lyon named Thibault, who fell 40 feet (12 meters) from a balcony four years ago, leaving him paralyzed from the shoulders down.

How it worked: Thibault had surgery to place two implants, each containing 64 electrodes, on the parts of the brain that control movement. Software then translated the brain waves read by these implants into instructions for movement. The development of the exoskeleton, by Clinatec and the University of Grenoble, is described in a paper in The Lancet this week.

Overview: Mind uploading is my favorite!

The Carboncopies Foundation is starting The Brain Emulation Challenge.


With the availability of high throughput electron microscopy (EM), expansion microscopy (ExM), Calcium and voltage imaging, co-registered combinations of these techniques and further advancements, high resolution data sets that span multiple brain regions or entire small animal brains such as the fruit-fly Drosophila melanogaster may now offer inroads to expansive neuronal circuit analysis. Results of such analysis represent a paradigm change in the conduct of neuroscience.

So far, almost all investigations in neuroscience have relied on correlational studies, in which a modicum of insight gleaned from observational data leads to the formulation of mechanistic hypotheses, corresponding computational modeling, and predictions made using those models, so that experimental testing of the predictions offers support or modification of hypotheses. These are indirect methods for the study of a black box system of highly complex internal structure, methods that have received published critique as being unlikely to lead to a full understanding of brain function (Jonas and Kording, 2017).

Large scale, high resolution reconstruction of brain circuitry may instead lead to mechanistic explanations and predictions of cognitive function with meaningful descriptions of representations and their transformation along the full trajectory of stages in neural processing. Insights that come from circuit reconstructions of this kind, a reverse engineering of cognitive processes, will lead to valuable advances in neuroprosthetic medicine, understanding of the causes and effects of neurodegenerative disease, possible implementations of similar processes in artificial intelligence, and in-silico emulations of brain function, known as whole-brain emulation (WBE).

Identification of a novel population of neuromedin S expressing neurons in the ventral tegmental area that promote morphine-elicited behavior

New in JNeurosci: Researchers identified a new subset of neurons in mice that morphine may interact with to influence behavior. This neuron population could be a promising new opioid addiction treatment target.

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Opioid use disorder constitutes a major health and economic burden, but our limited understanding of the underlying neurobiology impedes better interventions. Alteration in the activity and output of dopamine (DA) neurons in the ventral tegmental area (VTA) contributes to drug effects, but the mechanisms underlying these changes remain relatively unexplored. We used translating ribosome affinity purification and RNA sequencing to identify gene expression changes in mouse VTA DA neurons following chronic morphine exposure. We found that expression of the neuropeptide neuromedin S (Nms) is robustly increased in VTA DA neurons by morphine. Using an NMS-iCre driver line, we confirmed that a subset of VTA neurons express NMS and that chemogenetic modulation of VTA NMS neuron activity altered morphine responses in male and female mice. Specifically, VTA NMS neuronal activation promoted morphine locomotor activity while inhibition reduced morphine locomotor activity and conditioned place preference (CPP). Interestingly, these effects appear specific to morphine, as modulation of VTA NMS activity did not affect cocaine behaviors, consistent with our data that cocaine administration does not increase VTA Nms expression. Chemogenetic manipulation of VTA neurons that express glucagon-like peptide, a transcript also robustly increased in VTA DA neurons by morphine, does not alter morphine-elicited behavior, further highlighting the functional relevance of VTA NMS-expressing neurons. Together, our current data suggest that NMS-expressing neurons represent a novel subset of VTA neurons that may be functionally relevant for morphine responses and support the utility of cell type-specific analyses like TRAP to identify neuronal adaptations underlying substance use disorder.

Significance Statement The opioid epidemic remains prevalent in the U.S., with more than 70% of overdose deaths caused by opioids. The ventral tegmental area (VTA) is responsible for regulating reward behavior. Although drugs of abuse can alter VTA dopaminergic neuron function, the underlying mechanisms have yet to be fully explored. This is partially due to the cellular heterogeneity of the VTA. Here, we identify a novel subset of VTA neurons that express the neuropeptide neuromedin S (NMS). Nms expression is robustly increased by morphine and alteration of VTA NMS neuronal activity is sufficient to alter morphine-elicited behaviors. Our findings are the first to implicate NMS-expressing neurons in drug behavior and thereby improve our understanding of opioid-induced adaptations in the VTA.

Biohacker Takes Ketamine and Tracks His Brain With Surprising Results

Bryan Johnson took ketamine and monitored his brain activity for 15 days, recording the experience and sharing about it on X.

Johnson is a 47-year-old longevity-obsessed entrepreneur, known for sharing biohacking content across his social media channels. His most recent health experiment involved treatment with the popularized horse tranquilizer.

As he shared in a tweet, he wanted to test what happens to the brain before, during, and after ketamine treatment.

Ketamine has gained popularity as a fast-acting treatment for depression, PTSD, and chronic pain. Unlike traditional antidepressants, it works quickly by targeting the brain’s glutamate system to restore neural connections.

To monitor his brain activity, Johnson used his self-invented Kernel Flow—a form of non-invasive brain interface technology worn on the head.

S brain activity followed fixed, predictable patterns. After, he found his once-rigid thinking to be more flexible, varied, and open to new beliefs or ways of thinking. + Johnson likened his brain on ketamine to a global air traffic network, where each airport—or brain region—has consistent flight routes and traffic volumes.

“After ketamine, my brain’s activity patterns were completely scrambled. Instead of predictable routes between major hubs, traffic was rerouted to smaller, less-used airports across the U.S., Europe, and Asia,” he said in a tweet.

CARTA: The Biology of Hatred: Why Love Turns to Hatred and What We Can Do About It

Ancient texts warn of love turning into hatred, as seen in stories like Cain and Abel or “Et tu, Brute?” This talk explores the neurobiology of hatred based on the biology of love: the oxytocin system, attachment networks, and biobehavioral synchrony, which mature through mother-infant bonding and later support group solidarity and out-group hostility. Using this model, we developed Tools of Dialogue© for Israeli and Palestinian youth. After 8 sessions, participants showed reduced hostility, increased empathy, hormonal changes (lower cortisol, higher oxytocin), and lasting attitudes of compromise. Seven years later, these changes supported their peacebuilding efforts, showing how social synchrony can transform hatred into reciprocity and cooperation. Recorded on 02/14/2025. [Show ID: 40386]

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https://carta.anthropogeny.org/

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