Topic: GABAergic inputs

Neurons of the paraventricular thalamic nucleus (PVT) regulates emotional and motivational behavior via highly collateralized axon arbour innervating several forebrain areas. Maintaining an optimal excitation-inhibition balance is vital for PVT function, yet the sources of glutamatergic and GABAergic inputs are presently unclear. We identified subcortical glutamatergic and GABAergic inputs to the PVT by retrograde viral tracing in vGLUT2-Cre and vGAT-Cre mice, respectively. We found distinct retrogradely labelled cell groups containing purely vGLUT2+positive, purely vGAT+ or mixed neurons thro

Although traditionally thought to act primarily in the spinal cord, emerging evidence support important inhibitory functions by glycinergic transmission in the brain. In the ventral pallidum (VP), glycinergic afferents from the brainstem make synapses onto cholinergic interneurons to regulate arousal. Notably, VP is comprised of a heterogeneous population of GABAergic neurons, of which those that express somatostatin (SOM+) comprise a significant group and have been implicated in the control of sleep and wakefulness directly inhibiting cholinergic, glutamatergic and parvalbumin neurons. Here,

Hyperactivity is a persistent symptom of anorexia nervosa (AN) that often precedes occurrence of the disease, and constitutes a major barrier to recovery. Alteration of mesolimbic dopamine transmission has been hypothesized as a critical factor for the development and maintenance of AN and hyperactivity. However, the nature of dopamine dysfunction in AN, and the underlying mechanisms remain unclear. We therefore aimed at i) characterizing the impact of the activity-based anorexia (ABA) model on ventral tegmental area dopamine (VTADA) neurons and ii) determining whether restoring activity of VT