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Category: neuroscience

Neurons Use a Fast Structural Signal to Stabilize Communication

Researchers have uncovered a fast, structural mechanism that allows neurons to stabilize communication when synaptic function is disrupted.

Instead of relying on electrical activity, the brain uses physical rearrangements of postsynaptic receptors to signal the sending neuron to boost neurotransmitter release.

This rapid correction restores balance within milliseconds, ensuring that circuits supporting movement, learning, and memory remain functional.

The findings shed new light on how the brain maintains stability when communication falters.

Neurons can rapidly rebalance their communication using a structural signal rather than electrical activity, overturning long-held assumptions about how synapses maintain stability.

When neural spikes break time’s symmetry: Linking the information-theoretic cost of brain activity to behavior

What if we could peer into the brain and watch how it organizes information as we act, perceive, or make decisions? A new study has introduced a method that does exactly this—not just by looking at fine-grained neuronal spiking activity, but by characterizing its collective dynamics using principles from thermodynamics.

A team from Kyoto University and Hokkaido University developed a new statistical framework capable of tracing directional, nonequilibrium neural dynamics directly from large-scale spike recordings, enabling them to show how neurons dissipate entropy as they compute. Their findings reveal how neurons dynamically reshape their interactions during behavior and how the brain’s internal “temporal asymmetry” shifts during task engagement, shedding light on how efficient computation arises. The work is published in Nature Communications.

AI helps explain how covert attention works and uncovers new neuron types

Shifting focus on a visual scene without moving our eyes—think driving, or reading a room for the reaction to your joke—is a behavior known as covert attention. We do it all the time, but little is known about its neurophysiological foundation.

Now, using convolutional neural networks (CNNs), UC Santa Barbara researchers Sudhanshu Srivastava, Miguel Eckstein and William Wang have uncovered the underpinnings of covert attention, and in the process, have found new, emergent neuron types, which they confirmed in real life using data from mouse brain studies.

“This is a clear case of AI advancing neuroscience, cognitive sciences and psychology,” said Srivastava, a former graduate student in the lab of Eckstein, now a postdoctoral researcher at UC San Diego.

Role of brain’s immune system in social withdrawal during sickness

“I just can’t make it tonight. You have fun without me.” Across much of the animal kingdom, when infection strikes, social contact shuts down. A new study details how the immune and central nervous systems implement this sickness behavior.

It makes perfect sense that when we’re battling an infection, we lose our desire to be around others. That protects them from getting sick and lets us get much needed rest. What hasn’t been as clear is how this behavior change happens.

In the research published in Cell, scientists used multiple methods to demonstrate causally that when the immune system cytokine interleukin-1 beta (IL-1β) reaches the IL-1 receptor 1 (IL-1R1) on neurons in a brain region called the dorsal raphe nucleus, that activates connections with the intermediate lateral septum to shut down social behavior.

“Our findings show that social isolation following immune challenge is self-imposed and driven by an active neural process, rather than a secondary consequence of physiological symptoms of sickness, such as lethargy,” said study co-senior author.

Neurons use physical signals, not electricity, to stabilize communication

Every movement you make and every memory you form depends on precise communication between neurons. When that communication is disrupted, the brain must rapidly rebalance its internal signaling to keep circuits functioning properly. New research from the USC Dornsife College of Letters, Arts and Sciences shows that neurons can stabilize their signaling using a fast, physical mechanism—not the electrical activity scientists long assumed was required.

The discovery, published recently in Proceedings of the National Academy of Sciences, reveals a system that doesn’t depend on the flow of charged particles to maintain signaling when part of a synapse—the junction between neurons—suddenly stops working.

Maintaining this balance between neurons is essential for muscle control, learning and overall brain health. Failure to maintain this “homeostasis” has been linked to neurological conditions such as epilepsy and autism.

Fertility gene helps glioblastoma tumors survive chemotherapy and return after treatment, researchers discover

Research by University of Sydney scientists has uncovered a mechanism that may explain why glioblastoma returns after treatment, offering new clues for future therapies which they will now investigate as part of an Australian industry collaboration.

Glioblastoma is one of the deadliest brain cancers, with a median survival rate of just 15 months. Despite surgery and chemotherapy, more than 1,250 clinical trials over the past 20 years have struggled to improve survival rates.

Published in Nature Communications, the study shows that a small population of drug-tolerant cells known as “persister cells” rewires its metabolism to survive chemotherapy, using an unexpected ally as an invisibility cloak: a fertility gene called PRDM9.

Abstract: From synaptogenic to synaptotoxic

This issue’s cover features work by Alberto Siddu & team on the promotion of synapse formation in human neurons by free amyloid-beta peptides, in contrast to aggregated forms that are synaptotoxic:

The image shows a human induced neuron exposed to a nontoxic concentration of amyloid-beta42 peptide, revealing enhanced synaptogenesis, visible as synaptic puncta along the dendritic arbor.

Address correspondence to: Alberto Siddu, Lorry Lokey Stem Cell Building, 265 Campus Dr., Room G1015, Stanford, California 94,305, USA. Phone: 650.721.1418; Email: [email protected]. Or to: Thomas C. Südhof, Lorry Lokey Stem Cell Building, 265 Campus Dr., Room G1021, Stanford, California 94,305, USA. Phone: 650.721.1418; Email: [email protected].

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