Articles in 2017

Davis et al. report that fear memories can be critically regulated by parvalbumin-expressing interneurons in the basolateral amygdala. Silencing these interneurons following fear memory extinction caused a reemergence of fear expression that was accompanied by increased activation of fear-encoding neurons and fear-associated 3–6 Hz oscillations within a basolateral amygdala–prefrontal cortex circuit.

The authors show how predictive representations are useful for maximizing future reward, particularly in spatial domains. They develop a predictive-map model of hippocampal place cells and entorhinal grid cells that captures a wide variety of effects from human and rodent literature.

The precise underpinnings of Parkinson's disease and other disorders associated with the accumulation of α-synuclein are unclear. This study shows that PrP^C mediates α-synuclein-associated synaptic dysfunction and memory deficits. Blocking specific events in receptor biology rescued cognitive deficits in mice, suggesting new possibilities for intervention in synucleinopathies.

The mechanisms of gliotransmitter release and their impact on neuronal signaling have remained largely elusive. The authors describe two functionally non-overlapping v-SNARE-dependent astrocytic release pathways that oppositely control synaptic strength at presynaptic sites. Thus, astrocytes are able to fine-tune fast glutamatergic neurotransmission and control fundamental processes of synaptic communication.

Astrocytes differentially regulate excitatory and inhibitory synaptic transmission in the CeM, the major output nucleus of the amygdala. Astrocytes thereby reduce neuronal activity in the CeM and diminish fear expression in vivo. Therefore, astrocytes influence neural network activity and animal behavior through the regulation of specific synapses.

Dopamine has long been thought to contribute to neurodegeneration in Parkinson's disease. The authors show that dopamine-induced neuron death in the substantia nigra is dependent on α-synuclein and coincides with increased levels of α-synuclein oligomers. The results suggest a synergistic interaction between dopamine and α-synuclein that underlies neuronal vulnerability in disease.

Spinal cord injury causes life-threatening infections. The authors report that this is partially mediated by a maladaptive neuroendocrine reflex, extending from the spinal cord to the adrenal glands, where it blocks catecholamines while producing immunosuppressive corticosteroids. The effect depends on the spinal injury level, and normalization of hormones production by the adrenals rescued mice from pneumonia.

The authors identify the midcingulate cortex as a region that gates nociceptive plasticity without modulating basal nociception or the affective component of acute pain in mice. They identify a novel pathway from the midcingulate cortex to the posterior insula that recruits descending serotonergic projections to facilitate nociception.

A small population of brainstem noradrenaline neurons powerfully modulates global brain function, but how they regulate diverse—and at times opposing—functions is not clear. The authors report that a modular organization in this neuromodulatory system, coupled with context-dependent activation modes, controls the balance between opposing emotional and flexible learning states.

Esr1⁺ cells in the VMHvl are well known to influence female sexual behaviors. Here the authors find a surprising new role of this population in female aggression. They further reveal that the female VMHvl contains two molecularly and anatomically distinct subdivisions: one for aggression and one for sex.

Girardeau et al. show that coordinated reactivations of functionally connected neurons between the hippocampus and the basolateral amygdala occur during sharp wave–ripples of sleep following training on an aversive spatial task. These findings suggest a mechanism by which emotional memories are consolidated during sleep.

Long-range enhancer interactions regulate gene expression, yet how they influence CNS development and disease remains unclear. Glasgow et al. identified glia-specific elements and 3D chromatin architectures regulating NFIA expression during development. They also found that deletion of these enhancers suppresses NFIA expression and tumorigenesis in an in vivo glioma model.

Monkeys, like humans, normally have face domains in inferotemporal cortex; however, monkeys raised without exposure to faces do not develop face patches. Normally reared monkeys, like humans, preferentially look at faces, but face-deprived monkeys do not. These results highlight the importance of early experience for normal sensory and cognitive development.

Animals combine multiple cues to navigate the environment. By performing calcium imaging in fruit flies navigating in a virtual space, the authors show that information about recent visual experience and self-motion is separately encoded in parallel neural pathways in the central brain of Drosophila.

Using two-photon Ca²⁺ imaging in hippocampal area CA1 of Df(16)A^+/− mice, an animal model of 22q11.2 deletion syndrome, the authors found a reduction in spatial map stability compared to that in wild-type mice, as well as an absence of goal-directed place cell reorganization during goal-oriented spatial learning.

Neocortical resident microglia are long-lived cells. Füger et al. report that approximately half of these cells survive for the entire lifespan of a mouse. While microglial proliferation under homeostatic conditions is low, proliferation is increased in a mouse model of Alzheimer's disease.

Brain self-assembly is thought to be initiated by pioneer neurons whose identity is unknown. Rapti et al., addressing this long-standing mystery, uncover key steps in forming the brain-like nerve ring of C. elegans. Glia initiate the structure, using Netrin to guide pioneer neurons, whose identity is characterized. Glia and pioneer neurons then together direct follower-axon guidance using redundant guidance factors.

The amygdala central nucleus (CeA) has been implicated in feeding regulation, but the underlying circuit mechanisms are incompletely understood. The authors show, in mice, that GABAergic serotonin receptor 2a–expressing CeA neurons are active during eating and promote positive reinforcement and food consumption, partly through long-range inhibition of the parabrachial nucleus.

How GABAergic interneurons regulate segregation and integration among pyramidal cells to separate brain networks remains unclear. In this study, the authors show that subsets of chandelier cells in prelimbic area mediate directional inhibitory control of both local pyramidal neuron ensembles and global cortical subnetworks.

Recovery of the developing cerebellum after depletion of granule cells, the most plentiful neuron population, depends on adaptive reprogramming of neural progenitors to a new fate and a powerful cell–cell communication system that ensures re-establishment of the correct proportions of different cerebellar cell types and normal circuit formation.