Articles in 2015

The basal forebrain (BF) is important for sleep-wake control. In this study, the authors performed cell type–specific recording and manipulation of four genetically defined BF cell types in freely moving mice and mapped their synaptic connections in slices, providing a BF circuit diagram for sleep-wake control.

People with autism are known for their inflexible behavior. Using a perceptual learning protocol, the authors demonstrate initially efficient learning in observers with autism, followed by anomalously poor learning when the target location is changed (over-specificity). Furthermore, over-specificity can be circumvented by a specifically designed protocol that reduces stimulus repetitions.

The human ability to choose relies considerably on frontoparietal association cortex. Constructing unified perception from inconclusive sensory input also requires selection among alternatives. Combining fMRI with a novel visual stimulus, Brascamp and colleagues find evidence against frontoparietal involvement in such perceptual selection, instead suggesting choice capability in the visual system itself.

Contextual modulation is ubiquitous in sensory processing. This study shows that, in visual cortex, spatial contextual modulation for natural inputs is not well described by existing models. Instead, it can be explained by inference about statistical structure in images, with modulation evident only when images contain spatial redundancies.

In this study, the authors show that microglia play an important role in the propagation of pathogenic tau protein. In addition, the authors find that spread of the tau protein occurs via exosome secretion from these microglial cells.

The study of speech or vocal disorder resulting from neurological diseases lacks a model capable of recapitulating vocal learning. This study suggests that the vocal disorder associated with Huntington's disease is observed in transgenic zebra finches carrying the full-length human mutant huntingtin gene.

This protein quantitative trait analysis in monocytes evaluates cross-talk between Alzheimer risk loci and finds that the NME8 locus influences PTK2B, the CD33 risk allele leads to greater TREM2 expression, and the TREM1 risk allele is associated with a decreased TREM1/TREM2 ratio.

Optogenetic suppression of layer 4 in the sensory cortex reveals a surprising role for its activity in the cortical microcircuit: layer 4 suppresses the main cortical output layer—layer 5—through a direct translaminar inhibitory circuit. This translaminar inhibition sharpens spatial representations in the somatosensory cortex.

Using data from the Human Connectome Project, a single holistic multivariate analysis identified one strong mode of population co-variation: subjects were predominantly spread along a single ‘positive-negative’ axis linking lifestyle, demographic and psychometric measures to each other and to a specific pattern of functional brain connectivity.

How do fundamental synaptic processes in specific neuron populations drive behavior? A new study links a reduction of tonic inhibitory GABA current in a subset of central amygdala neurons to anxiety after fear conditioning.

A new study shows that an efficient allocation of sensory resources can lead to Bayesian estimates that are biased away from the prior, accounting for effects such as the bias toward oblique angles in orientation perception.

As conversion of odor signals to a two-dimensional map of activated glomeruli in the olfactory bulb is the key to odor recognition, decoding and deorphanizing of odorant receptors in the olfactory map is of great interest. Two genome-wide techniques now offer the ability to pair any odorant with its receptors.

We present a special issue focusing on recent advances in the understanding of the effects of stress on the nervous system and behavior, as well as the role of the nervous system in regulating responses to stress.

It is a truism that the brain influences the body and that peripheral physiology influences the brain. Never is this clearer than during stress, where the subtlest emotions or the most abstract thoughts can initiate stress responses, with consequences throughout the body, and the endocrine transducers of stress alter cognition, affect and behavior. For a fervent materialist, few things in life bring more pleasure than contemplating the neurobiology of stress.

In this Review, Hollon, Burgeno and Phillips discuss recent studies providing mechanistic insight into how stress alters circuitry involved in reward-related learning and motivation, as well as work examining how acute and chronic stress affect action selection in both rodents and humans.

The brain perceives and adapts to stressors via multiple interacting molecular mechanisms involving the cell surface, cytoskeleton and epigenetic regulation resulting in structural remodeling, with continually changing gene expression. Understanding mechanisms of plasticity and vulnerability facilitate development of intervention for anxiety and depressive disorders as well as age-related cognitive decline.

A mechanistic understanding of anxiety is required to advance the development of next-generation therapies for anxiety disorders. In this Review, Calhoon and Tye discuss recent insights into the circuit physiology driving anxiety-like behavior gained through the application of modern approaches in neuroscience.

In their Perspective, Hariri & Holmes consider unique features of translational research on stress-related disorders that have helped fuel a productive dialogue from bench to bedside and back, as well as sparked important advances in identifying novel risk biomarkers and therapeutic strategies.

Hodes et al. discuss mounting evidence in humans and rodent models of depression that causally links increased inflammation to depression. They take the perspective that heightened inflammation is a risk factor for depression and suggest targeted therapeutics to reduce inflammation as a novel approach to antidepressant treatment.

Severe stress impairs cognitive function, but enhances emotionality. This Review describes how stress triggers contrasting patterns of plasticity in the hippocampus, prefrontal cortex and amygdala, all brain areas that are involved in learning and memory. These features of stress-induced plasticity can have long-term consequences for the debilitating symptoms of stress-related disorders.