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A deep network is best understood in terms of components used to design it—objective functions, architecture and learning rules—rather than unit-by-unit computation. Richards et al. argue that this inspires fruitful approaches to systems neuroscience.
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.
Unexpected experiences often lead to strong memories. A new study by Krabbe and Paradiso et al. shows that vasoactive intestinal peptide (VIP)-expressing interneurons of the basolateral amygdala control associative learning and memory formation by gating aversive stimuli scaled by their unexpectedness.
Two new studies demonstrate the importance of awake imaging to investigate microglia–neuron interactions. These studies show that microglial dynamics are influenced by neuronal activity, and they provide evidence that norepinergic signaling plays an important role in this effect.
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.
Many studies focus on neural associations yet understanding the brain will ultimately depend on discovering the causal interactions underlying its functionality. Moving from association to causation will thus be essential for advancing neuroscience.
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.
Dube et al. generated an atlas of human brain circular RNA (circRNA) expression in individuals with and without Alzheimer disease (AD). They demonstrated circRNA expression correlates with AD severity, even before substantial clinical symptom onset.