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This paper identifies the evolutionarily conserved liprin-α protein family as key mediators of presynaptic assembly in human neurons. Their recruitment to sites formed by contacting neurons is the critical initial step that triggers presynaptic differentiation.

Cold sensor identities in peripheral somatosensory neurons remain obscure. We show that GluK2, a kainate-type glutamate-sensing chemoreceptor that mediates synaptic transmission in the brain, mediates the sensing of cold but not cool temperatures in mouse dorsal root ganglia neurons in the periphery. Thus, we identify GluK2 as a cold-sensing thermoreceptor.

The identity of receptors sensing cold temperatures in peripheral somatosensory neurons remains obscure. Cai et al. report that GluK2, a kainate receptor mediating synaptic transmission in the brain, is co-opted as a cold sensor in the periphery.

A real-time analysis system was developed for an up to 500-megabyte-per-second image stream. This system can extract activities from up to 100,000 neurons in larval zebrafish brains and enables closed-loop perturbations of brain-wide neural dynamics at cellular resolution.

This study investigates self-paced actions in freely foraging macaques. Findings highlight continuously evolving neural components that capture beliefs about latent reward dynamics, which are crucial for informed decision-making in a natural setting.

Astrocytes have important roles in disease and are difficult to modulate, owing to a paucity of known targets. Clayton et al. develop a screening platform to unbiasedly identify modulators of astrocyte reactivity. They discover that HDAC3 inhibitors regulate astrocyte transitions into their reactive phenotype in vitro and in vivo.

C9orf72 ALS/FTD polyGR and polyPR knock-in mice show cortical hyperexcitability and motor neuron loss accompanied by an increase in extracellular matrix proteins in the spinal cord that is conserved in patient iPS cell-derived neurons and is neuroprotective.

Sias et al. show that dopamine projections to the basolateral amygdala drive the reward learning that supports the predictions and inferences needed for adaptive decision-making.

Brain connections modulated by 534 deep-brain-stimulation electrodes revealed a gradient of circuits involved in dystonia, Parkinson’s disease, Tourette’s syndrome and obsessive-compulsive disorder. Together, these circuits begin to describe the human ‘dysfunctome’, a library of dysfunctional circuits that lead to various brain disorders.

Long COVID has remained an on-going public health issue in the years following the global pandemic. Here, we report blood–brain barrier disruption in patients with acute SARS-CoV-2 infection and brain fog, and patients presenting with long COVID, brain fog and cognitive decline, compared to those with long COVID without any neurological symptoms.

Hollunder et al. identify networks where deep brain stimulation reduces symptoms for Parkinson’s disease, Tourette’s syndrome, dystonia and obsessive-compulsive disorder. This revealed a fronto-rostral topography that segregates the frontal cortex.

Long COVID is a major public health issue since 2020 and exhibits frequent neurological symptoms. Greene et al. propose that brain fog results from leaky brain blood vessels and a hyperactive immune system, shedding light on this phenomenon.

Astrocytes have important roles in disease. However, modulation of their reactive state is challenging. Here the authors present a phenotypic in vitro screening platform they can leverage to identify chemical compounds able to modulate astrocyte reactivity in vitro and in vivo.

Using single-neuron recordings in patients with epilepsy, Kunz et al. show that stimulus-specific neurons activate together during hippocampal ripples when humans encode and retrieve associative memories.

Radke et al. found an interferon response in the brainstem nuclei of acute COVID-19 that, in addition to the inflammatory reaction, spreads throughout the vascular unit altering glial cells and resolves in late disease states in the absence of brain infection.

The Sehgal lab presents data showing that the non-cell autonomous pathway of glial lipid droplet formation occurs during sleep and helps to resolve neuronal reactive oxygen species (ROS). This promotes neuronal function after an active day. Hence, this pathway has an important physiological function beyond its previously described role in ROS-associated diseases, including Alzheimer’s disease.

Both caloric restriction and obesity affect autoimmune diseases. The activation of brainstem neurons in the ventrolateral medulla (VLM) with fasting suppresses experimental autoimmune diseases. Stimulation of VLM neurons alters T cell traffic by redistributing immune cells to bone marrow and reduces inflammatory cytokine production, thus providing therapy of experimental autoimmunity.