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The ability to filter out distracting sensory information is crucial to adaptive behavior. A primate study finds that prefrontal cortex is more important than parietal cortex in that function.
A report elucidates the widely recognized, but poorly understood, concept of gene-environment interaction, finding a molecular mechanism in the case of post-traumatic stress disorder: demethylation of a glucocorticoid response element in the stress response regulator FKBP5 that depends on both the risk allele and childhood trauma.
In a case of sex-linked epigenetic inheritance, paternal cocaine use results in a heritable increase in cortical Bdnf gene expression that confers a cocaine-resistant phenotype in male, but not female, progeny.
Two new studies provide experimental evidence of how ancient genomic duplications of synaptic genes provided the substrate for diversification that ultimately expanded vertebrate cognitive complexity.
A report in this issue of Nature Neuroscience demonstrates that stress in infancy leading to altered cortisol levels in childhood culminates in vulnerability to dysregulated affect in adolescent girls by biasing the functional dynamics of core neural regions mediating the generation and regulation of emotional responsiveness.
Using a new retrovirus-optogenetics technique, researchers have found that new neurons in the adult hippocampus are important for memory, but only at an immature stage, when they show enhanced synaptic plasticity.
Sustained activity of Hox5 transcription factors is needed for the development and maintenance of motor neurons that innervate the diaphragm, reports a study in Nature Neuroscience.
A study reconciling contradictory in vitro and in vivo data on neuroligins in synapse formation shows that cell-to-cell variability in neuroligin-1 levels, mediating competition for presynaptic inputs, regulates synapse density.
In this review, the authors examine the link between adult hippocampal neurogenesis and anxiety and depression. They propose that impaired pattern separation underlies the overgeneralization often seen in anxiety disorders.
Ligands for G protein–coupled receptor 88 (GPR88) have not yet been found. A new study finds that GPR88 is important in the physiology of dorsal striatal projection neurons, as well as in behaviors involving this brain region.
Genome-wide approaches are used to discover the RNA-binding targets of the amyotrophic lateral sclerosis (ALS) disease protein FUS/TLS. These studies reveal some shared targets with another ALS-linked RNA-binding protein, TDP-43, suggesting common pathogenic mechanisms.
A study reveals that medial entorhinal cortex layer III spiking dynamics shape the neocortical-hippocampal dialog during Up-Down state fluctuations in slow-wave sleep that may contribute to memory consolidation.
Variability in neuronal firing rates and spike timing can be modeled as doubly stochastic. A study now suggests that these phenomena could arise from a network built of deterministic neurons with balanced excitation and inhibition.
The authors review our understanding of the biological basis of resilience to stress. The review examines findings from both humans and animals and also discusses how this knowledge can help guide treatment for stress-related disorders.
Not only can the sleeping brain perceive sensory information, it can learn from this information, leading to changed behaviors the next day: it can come to associate a sound with a pleasant or unpleasant odor and react, both while still asleep and after waking, with a deeper or shallower breath. But classic ‘sleep learning’ remains just a dream.
Sleep consolidates memory. By cuing specific memories during sleep, a study now links this consolidation of memory to the replay of neuronal ensemble activity that occurs in the hippocampus during slow-wave sleep after learning.
During brain injury, mechanical injuries to neural cells initiate an apoptotic cascade through cardiolipin oxidation. Mitochondrially targeted electron scavenger compounds block this process, suggesting new therapeutic avenues.
Pathological alterations in Alzheimer's disease disrupt neuronal network function. An in vivo imaging study using a fluorescent reporter of neuronal activity finds dysfunction specifically in those neurons near amyloid plaques.
