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Pronounced Neuroplasticity in the Primary Visual Cortex of the Thirteen-lined Ground Squirrel During Hibernation

Hibernating animals can show neuroplasticity throughout the hibernation season. In ground squirrels, decreased dendritic arborization in the hippocampus, somatosensory cortex, and thalamus during deep hibernation (“torpor”) suggests that this neuroplasticity is a brain-wide phenomenon. However, the degree to which neuroplasticity occurs in the visual system is not clear. While transient retinal changes have been reported during torpor, neuroplasticity beyond the retina remains unknown. Here, we characterized hibernation-related neuroplasticity in the primary visual cortex (V1), the first cortical area to receive visual information, in the thirteen-lined ground squirrel (Ictidomys tridecemlineatus). We compared neuronal morphology in Golgi-stained samples from male and female hibernating or non-hibernating squirrels. For the hibernating squirrels, brain tissue was sampled during two different epochs: torpor and inter-torpor arousal. Dendritic arborization decreased during torpor in V1 layer 2/3 pyramidal neurons, manifesting as decreases in dendritic length, number, and complexity. These changes fully reversed during inter-torpor arousal, indicating that on average dendritic arbors grew by 0.75 mm (65%) over ∼1.5 hours. No morphological differences between hibernating and non-hibernating squirrels were apparent when compared 6 months after the hibernation season. We also found no neuroplastic changes in V1 layer 4 spiny stellate neurons, unlike in this cell type the somatosensory cortex. Together, this revealed, for the first time, hibernation-related neuroplasticity in V1 in support of a brain-wide mechanism but with area-specific differences. The speed and magnitude of this naturally occurring neuroplasticity could make ground squirrel V1 a powerful translational model system for conditions requiring neuroplasticity, such as recovery from stroke.

Significance Statement This study is the first demonstration of pronounced hibernation-related neuroplasticity in the primary visual cortex of ground squirrels. Layer 2/3 pyramidal neurons in the primary visual cortex (V1) reduced arborization during torpor. Within 1.5 hours after arousal from torpor, the arborization reversed to non-hibernation levels. The extent and speed of this naturally occurring neuroplasticity could make the relatively well-understood V1 of ground squirrels a powerful translational model system. Complementing insights on neuroplasticity in V1 during development, it has the potential to be leveraged for the study of treatment mechanisms and conditions requiring neuroplasticity, ranging from neurodegeneration to recovery after stroke.

Your Eyes Could Reveal Your Risk of Osteoporosis, Study Finds

The eyes are a window into our deeper health.

As the only outward extension of the central nervous system, these sensory organs may reflect not only the state of our brain and blood vessels, but also our very bones.

Population studies in Singapore and the UK have now revealed that a person’s risk of osteoporosis may be associated with how quickly their eyes are aging.

Brain ‘Zaps’ From Contact Lenses May Help Ease Depression, Mouse Study Shows

Scientists in South Korea have developed experimental contact lenses designed to send electrical signals through the retina and into brain regions linked to mood. In mice, the technology appeared to improve depression-like behaviour.

The idea sounds futuristic: a contact lens that could one day help treat depression by stimulating the brain through the eye. The work is still at a very early stage, with findings so far limited to a single mouse study.

The eye is already one of the body’s most useful access points for medical technology.

This Gene Is Linked to Lower Alzheimer’s Risk — And We May Finally Know Why

There’s something special about the APOE2 variant of the APOE (apolipoprotein E) gene: People who carry it tend to live longer, and they have a lower risk of developing Alzheimer’s disease.

Scientists are still trying to figure out why, and now, they have a new lead.

A team led by researchers at the Buck Institute for Research on Aging in the US set out to answer that question using human stem cell-derived neurons and mouse studies.

A new imaging approach captures brain activity across nine cell types at once

Scientists at the Max Planck Florida Institute for Neuroscience (MPFI), in collaboration with ZEISS and MetaCell, have developed a powerful new imaging pipeline called Neuroplex. As described in a paper published in eLife, the technique allows simultaneous monitoring of the activity of up to nine distinct neuronal populations in freely moving mice, dramatically accelerating the pace of scientific exploration into how the brain controls behavior.

For years, neuroscientists linking brain activity to behavior have faced a fundamental limitation: Miniscopes, the tiny head-mounted microscopes used to observe neural activity in behaving animals, could capture neural activity, but couldn’t reliably distinguish more than two different types of brain cells at a time.

“To understand the brain, we need to link patterns of activity in specific neurons to behavior,” stated lead author Dr. Mary Phillips. “We can readily use labels to color-code different populations of neurons, but when using miniscopes to correlate neural activity to behavior, we couldn’t distinguish more than two of these populations. This made it difficult to compare the activity across multiple cell types and circuits to understand how specific circuits regulate behavior.”

A cancer drug called saracatinib just switched failing brain synapses back on in Alzheimer’s mice — memory returned with them

When researchers at Yale gave a shelved cancer drug to old mice whose brains were already riddled with Alzheimer’s-like damage, the animals started remembering again. Synapses that had gone quiet flickered back to life. Proteins that mark healthy brain connections climbed toward normal levels. And when the drug was taken away, the cognitive gains stuck.

The drug is saracatinib, originally developed by AstraZeneca under the code name AZD0530 to treat solid tumors. It never panned out for cancer. But a team led by Stephen Bhatt and Christopher van Dyck at Yale School of Medicine recognized that its molecular target, an enzyme called Fyn kinase, plays a central role in how amyloid-beta destroys synapses in Alzheimer’s disease. Their work, published across several peer-reviewed studies between 2015 and 2020, has made saracatinib one of the more closely watched examples of drug repurposing in neuroscience. As of mid-2026, the compound’s preclinical results remain striking, but its clinical story is more complicated.

How early brain activity may shape speech-linked circuits before babies ever speak

Communication begins long before children learn to speak. Researchers at National Yang Ming Chiao Tung University (NYCU) in Taiwan have now uncovered how early brain activity helps build developing communication circuits via regulating FOXP2/Foxp2, a gene linked to human speech and communication disorders.

Published in EMBO Reports, the study presents an integrated framework linking neural activity, vocal circuit development, and activity-dependent regulation of Foxp2 in early life. The researchers studied neonatal mice, which emit ultrasonic vocalizations when separated from their mothers. These vocalizations are widely used to study early social communication and neurodevelopmental disorders.

Using advanced activity tagging, live neural recording, and circuit manipulation techniques, the NYCU team identified a previously underappreciated communication circuit linking the ventromedial prefrontal cortex (vmPFC) and the striatum.

New Brain “Bypass” Technology Could Transform Treatment for Neurological Disorders

A new technology called LinCx allows scientists to create custom electrical connections between neurons with high precision. Researchers say it may help treat disorders caused by damaged brain circuits. Damage to brain circuits plays a major role in many neurological disorders. Researchers at Duk

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