Volume 17 Issue 12, December 2016

Sean Hill explains why the growing importance of data-intensive neuroscience makes it crucial for the community to establish minimal metadata standards

Transplanted embryonic neurons can functionally replace ablated neurons in the primary visual cortex in adult mice.

Reductions in the response of the amygdala to dishonesty predict the escalation of self-serving dishonesty.

Following injection into the brain, different strains of tau aggregates induce different presentations of tau neuropathology in a mouse model of tauopathy.

This study suggests that brain-derived neurotrophic factor (BDNF) is released from dendritic spines in response to activity and acts in an autocrine manner to mediate structural plasticity of the spine from which it was released.

Cholinergic neurons in the basal forebrain of mice influence the intake of food and body weight by regulating appetite suppression.

In rats, stress promotes alcohol use by altering chloride gradients across the membranes of GABAergic neurons in the ventral tegmental area.

The properties and location of synaptic integrins put them in an ideal position to transduce signals from the extracellular matrix to intracellular signalling pathways. Park and Goda, here, describe the mechanisms underlying integrin-mediated synapse regulation and its contributions to development, plasticity and disease.

Mirror neurons transform sensory representations of others' behaviour into the observers' motor or visceromotor representations of that behaviour. In this Review, Giacomo Rizzolatti and Corrado Sinigaglia describe how the mirror mechanism is also likely to be involved in both action and emotion processing.

Viral entry into the CNS and infection of neural cells pose a specific challenge for the immune system: how to eradicate the invading pathogen without disrupting neuronal circuits. Rall and colleagues outline the host immune response to CNS viral infection and consider the possible consequences of non-lytic viral clearance in the brain.

The cognitive abnormalities observed in Alzheimer disease (AD) may be linked to alterations in oscillatory rhythmic activity and neuronal network hypersynchrony. Palop and Mucke review these links and explore how countering these network abnormalities and interneuron dysfunction may hold therapeutic potential for AD.