Boston, Mass. — Interoception is the awareness of our physiological states; it’s how animals and humans know they’re hungry or thirsty, and how they know when they’ve had enough to eat or drink. But precisely how the brain estimates the state of the body and reacts to it remains unclear. In a paper published in the journal Neuron, neuroscientists at Beth Israel Deaconess Medical Center (BIDMC) shed new light on the process, demonstrating that a region of the brain called the insular cortex orchestrates how signals from the body are interpreted and acted upon. The work represents the first steps toward understanding the neural basis of interoception, which could in turn allow researchers to address key questions in eating disorders, obesity, drug addiction, and a host of other diseases.

Using a mouse model his lab developed at BIDMC, Mark Andermann, PhD, principal investigator in the Division of Endocrinology, Diabetes and Metabolism at BIDMC and Associate Professor of Medicine at Harvard Medical School, and colleagues recorded the activity of hundreds of individual brain cells in the insular cortex to determine exactly what is happening as hungry animals ate.

The team observed that when mice hadn’t eaten for many hours, the activity pattern of insular cortex neurons reflected current levels of hunger. As the mice ate, this pattern gradually shifted over hours to a new pattern reflecting satiety. When mice were shown a visual cue predicting impending availability of food — akin to a person seeing a food commercial or a restaurant logo — the insular cortex appeared to simulate the future sated state for a few seconds, and then returned to an activity pattern related to hunger. These findings provided direct support for studies in humans that hypothesized that the insular cortex is involved in imagining or predicting how we will feel after eating or drinking.

Researchers reverse stroke damage in animal model using stem cell exosomes.

Expanding upon previous work that developed a treatment using a type of extracellular vesicles known as exosomes—small fluid-filled structures that are created by stem cells—investigators at the University of Georgia (UGA) present brain-imaging data for a new stroke treatment that supported full recovery in swine, modeled with the same pattern of neurodegeneration as seen in humans with severe stroke. Findings from this new study were published recently in Translational Stroke Research through an article titled “Neural Stem Cell Extracellular Vesicles Disrupt Midline Shift Predictive Outcomes in Porcine Ischemic Stroke Model.”

Amazingly, it’s been almost a quarter-century since the first drug was approved for stroke. Yet, what’s even more striking is that only a single drug remains approved today, so having a greater understanding of the molecular mechanisms that underlie stroke cases should lead to new therapies that could provide dramatic improvements in patient outcomes.

The researchers at UGA’s Regenerative Bioscience Center report the first observational evidence during a midline shift—when the brain is being pushed to one side—to suggest that a minimally invasive and nonoperative exosome treatment can now influence the repair and damage that follow a severe stroke.

A molecule produced by the brain that activates the same receptors as marijuana is protective against stress by reducing anxiety-causing connections between two brain regions, Vanderbilt University Medical Center researchers report.

This finding, published today in Neuron, could help explain why some people use marijuana when they’re anxious or under stress. It could also mean that pharmacologic treatments that increase levels of this molecule, known as “2-AG,” in the brain could regulate anxiety and depressive symptoms in people with stress-related anxiety disorders, potentially avoiding a reliance on medical marijuana or similar treatments.

When mice are exposed to acute stress, a break in an anxiety-producing connection between the amygdala and the frontal cortex caused by 2-AG temporarily disappears, causing the emergence of anxiety-related behaviors.

https://www.usf.edu/…/neuroscientists-discover-brain-pressu…

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Researchers at the University of South Florida have discovered a novel feedback pathway from the brain to the eye that modulates eye pressure – a significant advancement in the effort to diagnose and treat glaucoma. Glaucoma is associated with increased pressure in the eye due to a reduce ability of the eye to maintain proper fluid drainage. The heightened pressure applies mechanical strain to the optic nerve as the nerve exits the eye, resulting in vision loss and potential blindness.

It has long been hypothesized that brain pressure might also play a role in glaucoma because the amount of strain on the optic nerve depends not just on eye pressure, but the difference in pressure between the eye and brain. The groundbreaking study published in the Journal of Physiology shows, for the first time, that eye and brain pressure are physiologically connected. The neuroscientists came to this conclusion by altering brain pressure in animal models and noting changes in the fluid drainage properties of the eye that could be blocked by chemicals that eliminate feedback signals from the brain. Interestingly, the eye’s ability to clear fluid changed in a manner that restored a healthy pressure difference across the optic nerve.

Neuroregeneration entails not only neurogenesis, but also regrowth of lost connections and birth of non-neuronal cells. While adult neurogenesis in humans is only known to occur definitively in a few precisely circumscribed regions of the brain, work in other species suggests that science has only scratched the surface of the full regenerative potential of our own nervous systems.

The serotonergic system has widely been shown to control many aspects of neuroregeneration. In some regions, it facilitates neurogenesis, while in others, it seems to inhibit it. In the case of inhibition, a recent example has been published in PLOS Biology. The authors used a zebrafish model of Alzheimer’s disease to show that amyloid-induced interleukin-4 (IL4) promotes neurogenic stem cell proliferation by suppressing the production of serotonin. In these animals, there is a unique neuro-immune interaction through which IL4 secreted by dying neurons activates microglia. In turn, microglia reciprocate by revving up neural stem cell proliferation.