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Astrocytes are emerging as causal or modulating factors in diverse neurological disorders. Two papers published in Nature Neuroscience in 2007 revealed astrocytes as causally contributing to motor neuron loss in amyotrophic lateral sclerosis, thereby challenging the longstanding neuron-centric view of neurodegenerative disease.
In this issue of Nature Neuroscience, Kim and colleagues report that corticotropin-releasing factor neurons in the paraventricular nucleus, known essential regulators of the neuroendocrine axis, encode the valence of environmental stimuli through a bidirectional strategy and modulate animals’ immediate behavioral responses.
Considerations of optimality have served perceptual neuroscience well, but accumulating evidence suggests that optimal goals can be achieved by heuristic means. Theory that embraces this is key to uncovering the neural basis of perceptual behavior.
Disproportionate reactions to unexpected stimuli and greater attention to perceived threat are cardinal symptoms of post-traumatic stress disorder. Computational psychiatry helps explain how these responses develop and result from abnormalities in learning and prediction during and after traumatic events.
Excessive synapse elimination during adolescence and early adulthood has long been hypothesized to underpin the emergence of schizophrenia. A new study reports that induced microglia-like cells derived from schizophrenia patients display increased synapse engulfment, which may be partly mediated by a genetic schizophrenia-risk variant.
Geneticists are pushing for ever-greater sample sizes to gain insight into the genetic variation that contributes to psychiatric disorders. Two new genome-wide association studies leverage this approach to provide broad, population-level perspectives on the genetic basis for major depressive disorder and the shared genetic risk that underlies multiple disorders.
Variability is a ubiquitous aspect of neural recordings. In an influential paper, Churchland et al. (2010) compiled data from many cortical areas to demonstrate that variability generally decreases upon presentation of a stimulus. What are the implications of this finding?
Volterra et al. review evidence that astrocyte-generated signals participate in recruitment and function of neuronal networks underlying memory performance and that signal abnormalities under pathological conditions contribute to cognitive impairment.
Experience unfolds continuously in time, but we remember discrete sequences of events. In this issue of Nature Neuroscience, Montchal et al. describe brain activity patterns that predict how well people remember precisely when recent events occurred. Converging evidence suggests that homologous neural machinery structures temporal representations in rats and people.
In 2008, Vyazovskiy et al. published a seminal study demonstrating that sleep induces a widespread downscaling of synapses that counters the synaptic upscaling that occurred during prior wakefulness. The study laid the groundwork for current research into the ‘where’ and ‘when’ of homeostatic neuronal network regulation during sleep.