Articles in 2017

Central amygdala directs behavioral responses to emotionally salient stimuli. While most studies have focused on aversive responses, some central amygdala neurons promote feeding and are positively reinforcing.

Upon injury of the developing mouse cerebellum, endogenous repair mechanisms can heal the brain and prevent behavioral motor deficits. At the right time, with the right cues, the brain can repair itself.

Inputs to the central complex, the navigation center of Drosophila, are strongly modulated by the visual stimulus history. These history effects carry forward to bias turning behavior when flies choose between two visual stimuli.

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.

This paper reports the availability of a new Resource with RNA-seq, DNA methylation and H3K9Ac QTL results from 411 brain samples. Many xQTL SNPs influence multiple molecular features, and the authors observe epigenetic mediation of eQTLs in some cases. Reanalyzing GWAS with an xQTL-weighted approach detected 20 new CNS disease susceptibility loci.

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.

What is the basis for the feeling that someplace or someone is familiar? Molas et al. have identified brain structures involved in signaling familiarity, a necessary element for the expression of preference for novelty.