Articles in 2011

Here the authors identify NCKX4, a potassium-dependent Na⁺/Ca²⁺ exchanger as being necessary for rapid response termination and proper adaptation of vertebrate olfactory sensory neurons. They also report that Nckx4^−/− mice have a reduced ability to locate an odorous source and have lower body weights.

The authors report that GABA transporter 1 (GAT-1) cation currents directly increase GABAergic neuronal excitability and synaptic GABA release in the periaqueductal gray (PAG), and that these GAT-1 changes contribute to PAG-mediated signs of opioid withdrawal.

Loss of FMR1 gene function results in fragile X syndrome. Here, the authors demonstrate that the Drosophila fragile X homolog dFMR1 is involved in the RNA editing pathway via interaction with the enzyme dADAR and suggest that proper NMJ synaptic architecture requires modulation of dADAR activity by dFMR1.

The orbitofrontal cortex (OFC) has been hypothesized to carry information regarding the value of expected rewards. Such information could be used for generating instructive error signals conveyed by dopamine neurons. Here the authors report that this is indeed the case. However, contrary to the simplest hypothesis, OFC lesions did not result in the loss of all value information. Instead, lesions caused the loss of value information derived from model-based representations.

This study reports a double dissociation in the neuronal correlates of value-based decision making in monkey prefrontal cortex, with orbitofrontal cortex neurons encoding choice value relative to recent choice values, while anterior cingulate cortex neurons flexibly encode multiple decision parameters and reward prediction errors using a 'common valuation currency'.

This review addresses the issues that attend gene discovery in autism spectrum disorders (ASDs). It summarizes recent findings in human genetics and their relevance to models of pathology, highlights the issues raised by the apparent convergence of ASD genetic risks with distinct psychiatric disorders, and considers the interaction of neurobiology and genetics in our understanding of social disability syndromes.

DNA methylation in the context of epigenetics occurs on the 5' position of cytosine, which can be further oxidized by enzymes from the Ten-eleven translocation (Tet) family, resulting in 5-hydroxymethylcytosine (5-hmC). In the context of embryonic stem cells, Tet and 5-hmC DNA act in an alternate epigenetic state that regulates epigenetic programming and stem cell differentiation. Here, the authors describe the epigenomic profiling of 5-hmC in mouse and human brain across different time periods during development and aging.

People tend to remain overly optimistic even when faced with information about a gloomy future. A study now shows that people are selectively worse at incorporating information about a worse-than-expected future. It also describes the learning signals in the brain that correlate with this bias.

A new study dissects ephrinB reverse signaling and identifies separate intracellular pathways regulating dendritic and synaptic development.

Blood vessels in the nervous system are not simply inert bystanders that only support the metabolic needs of neurons. We present a focus on neurovascular interactions that highlights our emerging knowledge of how these interactions shape neuronal function both in health and disease.

Neurons form synapses with oligodendrocyte precursor cells (OPCs) that may control their maturation and myelination. Key signaling molecules regulating glutamate receptors at neuronal synapses also act in OPCs, but to opposite effect.

Patchy variation in odor-evoked electrical activity in the human olfactory epithelium is found to correlate with stimulus pleasantness. This finding depends on a new technique for recording directly from awake humans.

This perspective discusses newly discovered mechanisms leading to cellular ionic imbalances, as well as underappreciated signaling cascades that mediate cell death and that may add to the traditional glutamatergic mechanisms to which ischemic brain injury is ascribed. An integrated consideration of such new mechanisms may aid in formulating better therapies.

This review focuses on recent breakthroughs in understanding the biology of CNS pericytes and their role in the CNS in both health and disease.

Blood vessels in the CNS have traditionally been considered neutral bystanders that passively adapt in response to the needs of neural cells. This review surveys recent evidence that blood vessels actively participate in the pathogenesis of neurological disorders and the implications of this work for therapy.

There remains an urgent need to develop new strategies and therapies to help protect the brain from ischemic cell death. In this perspective, the authors suggest that learning more about the mechanisms that underlie brain self-preservation and developing multifaceted approaches that act on multiple pathways involved in both cell death and neuroprotection may advance our efforts to treat stroke.

Brain tumor stem cells (BTSCs) stimulate angiogenesis and may also directly contribute to tumor vasculature. The authors review the codependence of BTSCs and the perivascular niche and how this may inform new therapeutic approaches.

In this behavioral study, the authors demonstrate how increased attention can sometimes lead to lower subject confidence, leading subjects to become more conservative in making decisions during a visual perception task.