An orbitocortical-thalamic circuit suppresses binge alcohol-drinking.

Alcohol consumption remains a significant global health challenge, causing millions of direct and indirect deaths annually. Intriguingly, recent work has highlighted the prefrontal cortex, a major brain area that regulates inhibitory control of behaviors, whose activity becomes dysregulated upon alcohol abuse. However, whether an endogenous mechanism exists within this brain area that limits alcohol consumption is unknown.

A neuronal coping mechanism linking stress-induced anxiety to motivation for reward.

Stress coping involves innate and active motivational behaviors that reduce anxiety under stressful situations. However, the neuronal bases directly linking stress, anxiety, and motivation are largely unknown. Here, we show that acute stressors activate mouse GABAergic neurons in the interpeduncular nucleus (IPN).

A loss of Pdxk model of Parkinson disease in Drosophila can be suppressed by Buffy.

Background: The identification of a DNA variant in pyridoxal kinase (Pdxk) associated with increased risk to Parkinson disease (PD) gene led us to study the inhibition of this gene in the Dopa decarboxylase (Ddc)-expressing neurons of the well-studied model organism Drosophila melanogaster. The multitude of biological functions attributable to the vitamers catalysed by this kinase reveal an overabundance of possible links to PD, that include dopamine synthesis, antioxidant activity and mitochondrial function. Drosophila possesses a single homologue of Pdxk and we used RNA interference to inhibit the activity of this kinase in the Ddc-Gal4-expressing neurons.

knockdown phenotypes are suppressed by and exacerbate degeneration in a model of Parkinson disease.

Background: Bax inhibitor-1 (BI-1) is an evolutionarily conserved cytoprotective transmembrane protein that acts as a suppressor of -induced apoptosis by regulation of endoplasmic reticulum stress-induced cell death. We knocked down in the sensitive () expressing neurons of to investigate its neuroprotective functions. We additionally sought to rescue the -induced phenotypes by co-expression with the pro-survival and determined the effect of knockdown on the neurodegenerative α--induced Parkinson disease (PD) model.