JNeurosci: Highlights From the August 17 Issue
Check out these newsworthy studies from the August 17, 2016, issue of JNeurosci. Media interested in obtaining the full text of the studies should contact media@sfn.org.
Genetic Reprogramming of Supporting Cells in Cochlea Generates New Hair Cells
Hair cells — auditory receptors located in the cochlea — fail to regenerate when damaged, and hair cell loss is the leading cause of hearing disorders. Supporting cells in the cochlea can differentiate into hair cells, but this often depletes the population of supporting cells. Researchers have found a way to genetically reprogram supporting cells in the mouse cochlea so that they both proliferate and differentiate into hair cells, which may suggest new ways to stimulate hair cell regeneration in hearing disorders.
Corresponding author: Huawei Li, lihuawei63@gmail.com
Changes in Amygdala Activity Can Both Enhance and Decrease Social Behavior in Monkeys
Studies in nonhuman primates indicate that damage to the amygdala — a structure deep within the brain involved in emotion and learning — can impair social interactions. But a new study in macaques finds that temporarily blocking activity in specific subregions of the amygdala enhanced social behavior, while activating one of these regions decreased social interactions. This is the first study to assess the separate roles of the amygdala subregions in social behavior in primates.
Corresponding author: Ludise Malkova, malkoval@georgetown.edu
How Neural Activity Regulates Synaptic Vesicle Recycling
For efficient neurotransmission, neurons maintain a pool of neurotransmitter-containing synaptic vesicles, which are constantly recycled and reformed. Buildup of damaged proteins on vesicles can interfere with this recycling process and impair synaptic function. Working in cultured rat neurons, researchers uncovered the molecular pathway by which neural activity drives the breakdown of damaged proteins in order to prevent their buildup on vesicles.
Corresponding author: Clarissa Waites, cw2622@columbia.edu
Alzheimer’s Protein Needed for Normal Neural Development
The accumulation of beta-amyloid protein fragments in neurons is a pathological hallmark of Alzheimer’s disease. A growing body of research suggests aberrant interactions between the beta amyloid precursor — amyloid precursor protein (APP) — and other molecules may contribute to the disease, but the exact identities and roles of these molecules are unknown. Working in a moth model, researchers found APP interacts with a cell adhesion protein to help neurons migrate to the right targets during development. The study provides a framework to understand how alterations in APP and its interactions with other molecules may contribute to Alzheimer’s disease.
Corresponding author: Philip Copenhaver, copenhav@ohsu.edu
Brain Area Regulates Both Hormonal and Behavioral Response to Stress
The bed nucleus of the stria terminalis (BST) integrates stress signals from various areas of the brain, and dysregulation of this neural circuitry is implicated in stress-related psychiatric illness. Using optogenetic techniques, researchers blocked activity in a specific region of the BST in mice and found the mice had higher levels of stress hormones and gave up sooner (rather than actively trying to escape) during a stress test. The findings suggest impairment of this specific region may explain some of the features of stress-related illnesses.
Corresponding author: Jason J. Radley, jason-radley@uiowa.edu
The Journal of Neuroscience is published by the Society for Neuroscience, an organization of nearly 38,000 basic scientists and clinicians who study the brain and nervous system.
