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Recent studies reveal several groups of neurons that become activated upon anticipation or consumption of meals. These neurons constitute key components of the complex feedback system that prevents continuous feeding by mice.
Grid-firing fields of neurons in the entorhinal cortex are thought to require inputs encoding running speed. Glutamatergic projections from the medial septum may be one of the inputs that provide these speed signals.
Evidence reveals that humans share remarkably similar patterns of event-specific neural activity during spontaneous spoken recall. Posterior medial cortex appears to play a key role in transforming experience into memory.
An elegant study answers a long-standing question: how do correlations arise in large, highly interconnected networks of neurons? The answer represents a major step forward in our understanding of spiking networks in the brain.
Humans and animals can collect and maintain information that guides decisions, but how neural circuits achieve this is unknown. It seems neural populations may do so by passing through diverse states in many possible sequences.
During synaptic activation, the function of astrocyte endfeet depends on the vascular target: at the capillary, but not at the arteriole, a newly described P2X1R–phospholipase D2 pathway modulates prostaglandin E2 release and vessel dilation.
Recent experiments suggest that dishonesty can escalate from small levels to ever-larger ones along a 'slippery slope'. Activity in bilateral amygdala tracks this gradual adaptation to repeated acts of self-serving dishonesty.
Intellectual disabilities and associated neurodevelopmental disorders may result from rare genetic mutations. Ganna et al. show that these also help explain variability in educational attainment, a proxy for cognitive function.
Recent models studying loss of the mouse homolog of the autism-associated gene CHD8 show altered Wnt signaling, cell fate and proliferation. How do these findings shape our understanding of this disease?
A large DNA sequencing study of schizophrenia finds more evidence that rare inherited coding mutations across many genes contribute to risk of the disorder. This has important implications for geneticists and neuroscientists alike.
Recently, robust identification of hundreds of genetic variants associated with risk for neuropsychiatric disease has prompted new challenges in understanding their biological impact within an individual. The authors provide a framework for interpretation of genetic risk variants to uncover disease mechanisms and facilitate therapeutic development.
Animal models have failed to yield new treatments for psychiatric disorders. Some psychiatric disorders may result from pathology in plasticity mechanisms. Therefore, understanding plasticity mechanisms in model systems may provide insight into the disordered processes in patients.
Autism spectrum disorders are highly heterogeneous and include both idiopathic and syndromic forms. Sztainberg and Zoghbi discuss insights gained from studying syndromic autism spectrum disorders and their potential contribution to our understanding of the molecular pathways critical for normal cognitive and social development, as well as the relevance to idiopathic autism.
Functional studies of neuronal assemblies that encode memories have progressed dramatically due to recent technological advances. This review shows how a focus on assembly formation and consolidation provides a powerful conceptual framework to relate mechanistic studies of synaptic, neuronal and circuit plasticity to behaviorally relevant aspects of learning and memory.
While the relationship between motivation and sleep is intuitive, its behavioral and neural features are poorly understood. A new study tackles both issues, showing that dopaminergic neurons in the ventral tegmental area mediate this relationship.
The dorsal anterior cingulate cortex is one of the most beguiling regions of the brain. Understanding its essential function has become a holy grail for many cognitive neuroscientists. With this scrutiny has come contention. In this issue, two teams of neuroscientists with different views argue for their favored interpretation of neural activity in this region. Here, we provide some background and context for this debate.
A neural code for sequences needs to allow the recruitment of plasticity mechanisms that link successive items. New results suggest that this is achieved by coupling gamma band activity to specific phases of theta oscillations.
Neurons require lifelong maintenance of their transcriptional program, which includes stable expression of cell-type-specific identity genes. A study now shows that PRC2-mediated chromatin repression in adulthood is critical for the maintenance of neuronal identity gene expression and neuronal survival.
