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Category: neuroscience – Page 73

Human brains explore more to avoid losses than to seek gains

Researchers at the Weizmann Institute of Science traced a neural mechanism that explains why humans explore more aggressively when avoiding losses than when pursuing gains. Their work reveals how neuronal firing and noise in the amygdala shape exploratory decision-making.

Human survival has its origins in a delicate balance of versus exploitation. There is safety in exploiting what is known, the local hunting grounds, the favorite foraging location, the go-to deli with the familiar menu. Exploitation also involves the risk of over-reliance on the familiar to the point of becoming too dependent upon it, either through depletion or a change in the stability of local resources.

Exploring the world in the hope of discovering better options has its own set of risks and rewards. There is the chance of finding plentiful hunting grounds, alternative foraging resources, or a new deli that offers a fresh take on old favorites. And there is the risk that new hunting grounds will be scarce, the newly foraged berries poisonous, or that the meal time will be ruined by a deli that disappoints.

Treatment For Psychosis May Be ‘Fundamentally Flawed’, Study Finds

For decades, psychiatrists have treated psychosis as if it were separate conditions. People experiencing hallucinations and delusions might be diagnosed with schizophrenia, bipolar disorder, severe depression and related diagnoses, and receive completely different treatments based on diagnosis.

But new research suggests this approach may be fundamentally flawed.

Our latest study, published in JAMA Psychiatry, reveals that the brain changes driving psychotic symptoms are remarkably similar across these supposedly distinct mental health conditions. The findings could change how doctors choose treatments for the millions of people worldwide who experience psychosis.

New insights into the epigenetic processes via which neuroinflammation causes memory loss

Neuroinflammation, a prolonged activation of the brain’s immune system prompted by infections or other factors, has been linked to the disruption of normal mental functions. Past studies, for instance, have found that neuroinflammation plays a central role in neurodegenerative diseases, medical conditions characterized by the progressive degradation of cells in the spinal cord and brain.

When inflammation is taking place, cells release proteins that act as signals between immune cells, also known as cytokines. While some studies have linked a specific cytokine called interleukin-1 (IL-1) to changes in brain function, the mechanisms through which it could contribute to a decline in mental capabilities remain poorly understood.

Researchers at the University of Toulouse INSERM and CNRS recently carried out a study involving mice aimed at better understanding these mechanisms. Their paper, published in Nature Neuroscience, particularly focused on neuroinflammation elicited by the parasite Toxoplasma gondii (T. gondii), which is responsible for a well-known illness called toxoplasmosis.

How an autism-linked mutation reduces vasopressin and alters social behavior

A team of researchers has identified for the first time the mechanism linking a mutation in the Shank3 gene with alterations in social behavior. Using a mouse model carrying this autism-associated mutation, the study shows that vasopressin, a brain hormone essential for social relationships, is not properly released in the lateral septum.

The team is from the Cognition and Social Interactions laboratory, led by Félix Leroy at the Institute for Neurosciences, a joint center of the Spanish National Research Council (CSIC) and the Miguel Hernández University (UMH) of Elche.

The work, published in Nature Communications, demonstrates that the proper release of vasopressin in this region regulates social behaviors through two distinct receptor pathways: one controlling sociability and the other controlling social aggression, and that selective activation of these receptors can reverse deficits in social interaction without triggering unwanted aggressive responses.

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