Volume 26 Issue 12, December 2023

In 2022, we began a pilot to facilitate data sharing for manuscripts submitted to Nature Neuroscience. Here, we analyze its effects on research data availability and reflect on the importance of facilitating open science.

As Nature Neuroscience celebrates its 25th anniversary, we are having conversations with both established leaders in the field and those earlier in their careers to discuss how neuroscience has evolved, and where it is heading. This month, we are talking to Corey Harwell, Associate Professor of Neurology at the University of California, San Francisco (UCSF) School of Medicine. We spoke about the mentors who shaped his early interest in neuroscience, and how his lab lets their data lead them in interesting directions.

As Nature Neuroscience celebrates its 25th anniversary, we are having conversations with both established leaders in the field and those earlier in their careers to discuss how the field has evolved and where it is heading. This month, we are talking to Costantino Iadecola (Director and Chair of the Feil Family Brain & Mind Research Institute, Weill Cornell Medicine, NY, USA), a neurovascular biologist and physician interested in the roles of vasculature, hypertension and immune cells in ischemic stroke and neurodegenerative diseases.

George Aghajanian died on July 4, 2023 in Guildford, Connecticut, at the age of 91. An electrophysiologist and innovator, George was a much-loved mentor, colleague and friend. His laboratory captured the first in vivo recordings of serotonin, norepinephrine and dopamine neurons. For over half a century, George’s research at the Yale University School of Medicine opened new fields of discovery in neuroscience.

We discovered expression of SYNGAP1, which encodes the ‘synaptic’ protein SYNGAP1, within human cortical progenitors. In an organoid model of SYNGAP1 haploinsufficiency, cortical neurogenesis and neuronal network activity were disrupted. This finding reveals an unknown function for SYNGAP1 at early stages of development, providing a new framework for understanding the pathophysiology of autism spectrum disorder.

Recent discoveries highlight the skull bone marrow, linked to the CNS via osseous channels, as a key neuroimmune compartment. Here, the authors discuss the anatomy, functions and implications of this immune reservoir on CNS health and disease.

This paper characterizes two distinct philosophies underlying previous work on how Bayesian computations are linked to neural data, highlighting how different theories may be motivated by different tacit assumptions and thereby explain different data.

This study by Zielinski et al. used cryo-EM to compare Aβ fibril structures from mouse models to those from patients with Alzheimer’s disease. It revealed that tg-APP_ArcSwe mice exhibit fibrils resembling those predominantly found in sporadic Alzheimer’s disease cases.

Neuronal somata perform higher levels of aerobic glycolysis and lower levels of OXPHOS than terminals, which safeguards against oxidative damage.

Experiments in human cortical organoid and mouse models of SYNGAP1 haploinsufficiency, which is associated with autism spectrum disorder (ASD), reveal altered cortical neurogenesis, suggesting that a non-synaptic mechanism contributes to the disorder.

Nelson et al. report that the APOE-R136S mutation protects against APOE4-promoted Alzheimer’s disease pathologies, including phosphorylated Tau accumulation, neuroinflammation and neurodegeneration, in mouse and human neuron models.

The authors identify a cluster of ~160 peptidergic neurons in the mouse brainstem whose activity is necessary and sufficient for producing sound and controlling sound volume. These neurons form the final common pathway for vocalization.

The authors describe the connectivity, response profile and behavioral roles of two transcriptionally defined amygdala populations from separate embryonic lineages and show how responses of one population change with social experience.

What neurons encode when animals face a dangerous situation is unclear. Here, the authors show that the prefrontal cortex encodes both threat-specific information and a more general representation of the presence of danger.

Radulescu et al. show that homeostatic mechanisms that reduce cortical activity following overstimulation are dysregulated later in life, such that overstimulation results in synaptic strengthening, elevated activity and cognitive impairment.

This study applies topological analysis to hippocampal ripple waveforms, uncovering a low-dimensional continuum that encodes layer-specific synaptic input information. It also reveals how ripple waveforms vary during wakefulness, sleep and learning.

The authors show that neural activity and synaptic plasticity in the orbitofrontal cortex mediate multiple timescales of reinforcement learning (RL) for meta-RL, which parallels a form of meta-RL in artificial intelligence.

Parker et al. recorded neural activity in V1 of freely moving mice and freely gazing marmosets. In both species, neurons respond to gaze shifts in a temporal sequence, such that new visual input is processed in a ‘coarse’ to ‘fine’ manner.

McGinty and Lupkin show that value-based choices in monkeys are explained by multi-neuron activity patterns in the orbitofrontal cortex (OFC) that are not evident in single cells. Identifying this neural–behavioral link sheds light on the OFC’s role in decision-making.

Using direct intracranial recordings and modern speech AI models, Li and colleagues show representational and computational similarities between deep neural networks for self-supervised speech learning and the human auditory pathway.

Perl et al. show that in PTSD, hippocampal representations of autobiographical memories are similar across people with similar semantic content only for sad but not traumatic memories, pointing to altered brain state during traumatic memory recall.

The neuronal subtypes regulating the emotional component of learning and memory are not fully described. Here the authors provide a molecular atlas of the adult mouse amygdala and show the subsets of cells transcriptionally responsive to fear.