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Walking requires continual integrated information about the dynamic internal and external environment. This study reveals a pathway whereby the somatosensory cortex directly influences motor behavior based on integrated spatiotemporal information.
Zhou et al. show that the reward and context information of cocaine-associated memory is stored in selectively strengthened inter-engram connections from the ventral CA1 to the nucleus accumbens core, forming an ‘engram circuit’ that mediates memory recall.
Hartley et al. report the bidirectional remodeling of a basolateral amygdala-to-central amygdala neural circuit, where input onto corticotropin-releasing factor (CRF)-expressing and CRF-negative neurons is shaped by the acquisition and extinction of fear memory.
Qasim et al. describe neurons in the human entorhinal cortex that activate near the locations in space that a person is cued to recall during a memory task. These results show one way in which the cognitive map shifts according to memory demands.
The authors develop a deep learning approach that enables an efficient search of the input space to find the best stimuli for modeled neurons. When tested, these stimuli are most effective at driving their matching cells in the brain.
Forkosh, Karamihalev and colleagues present a framework for inferring stable traits from a broad range of behavioral readouts and apply it to capture biologically relevant individual differences in mice.
Findling, Skvortsova et al. find that a large fraction of non-greedy decisions that humans make in volatile environments do not stem from exploration but from the limited precision of learning, and further identify its neurophysiological correlates.
The Drosophila neuropeptide leucokinin mediates hunger- and thirst-dependent expression of learned behaviors. State-relevant selection of appropriate memory emerges from competition between leucokinin and other modulators onto dopaminergic neurons.
Human stem cell-derived microglia integrate into mouse brain, displaying transcriptome signatures of microglia directly isolated from human brain and providing a chimeric model to study human-specific aspects of Alzheimer’s disease and other brain diseases.
Chow et al. show that high blood levels of insulin in prediabetic conditions are linked to saturated insulin levels in the brain. Chronic insulin exposure leads to insulin resistance, cell cycle reentry and premature aging, corresponding to senescence-like pathological changes in neurons.
Krabbe, Paradiso et al. show that amygdala VIP interneurons are activated by instructive cues for associative learning. These interneurons provide a mandatory disinhibitory signal permitting plasticity in response to unexpected salient events.
Liu et al. show that microglial process surveillance is restrained in awake mice, and that reduced neuronal activity due to anesthesia, sensory deprivation or optogenetic inhibition increases microglial dynamics via norepinephrine signaling.
Stowell, Sipe et al. describe how norepinephrine signaling to microglia during wakefulness influences the dynamic movement of microglial processes, affecting both microglial interactions with neurons and experience-dependent plasticity.
In offspring exposed to THC in utero, molecular, synaptic and circuit reorganizations lead to a hyperdopaminergic phenotype and behavioral susceptibility. The neurosteroid pregnenolone restores both dopamine function and abnormal behavior.
Munji et al. analyzed the transcriptomes of endothelial cells from multiple organs and in neural tissue of neurological disease models. They identified a blood–brain barrier dysfunction module in seizure, multiple sclerosis, stroke and brain trauma.
The authors found that activity of the same ventral tegmental area dopaminergic axons in basal amygdala increased following learned cues predicting either food rewards or punishments, in a manner consistent with signaling of motivational salience.
The authors report that the ALS-associated gene FUS stimulates transcription of acetylcholine receptor subunit genes in subsynaptic myonuclei. ALS mutations distort this mechanism, inducing muscle-intrinsic toxicity that may contribute to dying-back motor neuronopathy.
Control of movements can be understood in terms of the interplay between a controller, a simulator and an estimator. Egger et. al. show that cortical neurons establish the same building blocks to control cognitive states in the absence of movement.
This manuscript describes the systematic investigation of epigenomic signatures discriminating between regenerative success and failure in dorsal root ganglia sensory neurons following axonal injury. This epigenomic map offers a tool to design novel approaches for neuronal repair.
Frank et al. find that a subregion in the zebrafish homolog of olfactory cortex maps odor space onto a representation of valence. Learning shapes this odor-to-valence map through plasticity processes that modify inhibition.