Articles in 2014

A study now provides proof of concept that restoration of Ras-Erk signaling during adulthood rescues cellular and cognitive phenotypes in mouse models of the genetic disorder Noonan syndrome.

December 2014 marks the 200th issue of Nature Neuroscience. We reflect on the history of the journal and the field.

A randomized clinical trial in older adults shows that high dietary intake of cocoa flavanols enhances memory performance on an object-recognition task and neural activity as assessed by functional magnetic resonance imaging in the dentate gyrus of the hippocampus, a region that is critical for learning and memory.

Patch-clamp recordings and imaging in retina show that electrical synapses between dendrites of neighboring ganglion cells transform spatial patterns of light activated synaptic input into a temporal population code.

The amygdala is known to play an important role in fear conditioning. In this Review, the authors discuss extended circuits beyond the amygdala mediating fear learning and expression, focusing on the neural coding mechanisms underlying these behaviors.

In this Review, Lüscher and Lüthi draw some parallels between anxiety and addiction disorders as diseases of the brain's emotional valence system. The authors present an update on the anatomy and heterogeneity of the fear and reward circuitries, analyze our understanding of the synaptic and cellular mechanisms thought to underlie the two conditions and discuss recent studies causally linking the resulting circuit dysfunctions and alterations in behavior.

Lecoq and colleagues introduce a two-photon microscope with two articulated arms that can image nearly any two brain regions, nearby or distant, simultaneously. They validate this new system by imaging calcium signals in two visual cortical areas in behaving mice, and find evidence suggesting activity fluctuations can propagate between cortical areas

The authors report an optical method involving simultaneous stimulation of single neurons using a red-shifted optogenetic probe and recording of population activity using a green fluorescent calcium sensor. They use this technique to manipulate individual place cells in CA1 during spatial navigation in a virtual reality environment.

The authors show that mice lacking Fragile X Mental Retardation Protein (FMRP) have disrupted neuronal migration during cortical development. FMRP-deficient mice also show altered excitatory-to-inhibitory balance early postnatally. They identify N-cadherin as a target of FMRP and show that re-expressing N-cadherin can rescue these phenotypes in FMRP-deficient mice.

The authors report that in mice, the cerebellum modulates the activity of the striatum via a disynaptic pathway to facilitate optimal motor control. Dysfunction of this pathway can contribute to dystonia.

Corticotropin-releasing factor (CRF) and dopamine (DA) are critical for stress and motivation, respectively. The authors show that CRF is synthesized in DA neurons and released in the ventral tegmental area, where it affects GABAergic inputs to DA neurons and mediates the motivational effects of nicotine withdrawal and escalation of nicotine intake.

Primate cortex can be organized with specialization and hierarchical principles, but presently there is little evidence for how it is organized temporally. Across six separate datasets, the authors find a hierarchical ordering of intrinsic fluctuation of spiking activity, with timescales that increase from sensory to prefrontal areas.

The counter-regulatory response (CRR) restores blood glucose levels after hypoglycemia. The authors identify a population of leptin receptor– and cholecystokinin-expressing neurons in the parabrachial nucleus of the hypothalamus that modulates the CRR. These neurons are activated by hypoglycemia, inhibited by leptin and project to the ventromedial hypothalamus.

Noonan syndrome (NS) is an autosomal dominant genetic disease that is co-morbid with cognitive deficits in a subset of patients. Using mouse models of NS, a study now shows that the synaptic plasticity and memory deficits in mouse models of NS are due primarily to the dysfunction in the MEK-Erk kinase pathways, and pharmacological intervention that alters MEK-Ras function can alleviate physiological and behavioral deficits in the mouse models of NS.

The many different behaviors mediated by the posterior parietal cortex (PPC) could arise from distinct specialized categories of neurons or from a single population of PPC neurons that is leveraged in different ways. The authors test this by studying rat PPC neurons during tasks involving multisensory decisions and conclude that a single network of neurons can support different behavioral demands.

This Resource article provides detailed expression data from the striatum and cerebral cortex of early prenatal human samples, ranging in age from 2 to 20 weeks post-conception. Using a number of different analyses, the authors describe the transcriptional, spatio-temporal expression and functional profile that distinguish human striatal from neocortical neurons while also elucidating some differences between human and mouse striatal development.

Fragile X Syndrome (FXS) patients and the mouse model of the disease are known to have increased neocortical network excitability and hypersensitivity to sensory stimuli. The current study describes dendritic ion channel dysfunction to underlie sensory hypersensitivity in the FXS mouse model, particularly due to the reduction and dysfunction of dendritic h- and BK_Ca channels. The study also shows pharmacological rescue of cortical hyperexcitability using BK_Ca channel openers.

Training macaque monkeys with distinct sets of shapes resulted in novel domain formation in inferotemporal cortex. The localization of these domains was similar across monkeys, regardless of set-training order. The stereotyped location of the training-induced domains suggests a pre-existing architecture, and the authors explored various possible proto-architectures.

Neuregulin 1 (NRG1) type III is a key mediator of Schwann cell development and myelination and is known to undergo proteolytic cleavage to produce an intracellular fragment. In this study, the authors show that this intracellular fragment of NRG1 modulates myelination by inducing the expression of a prostaglandin synthase (L-PGDS) which, in turn, leads to prostaglandin production and activation of GPR44.