Cocaine Enhances Gamma-Aminobutyric Acid Release From Reticular Thalamic Nucleus: Role of T-Type Calcium Channels

Abstract

Thalamic reticular nucleus (TRN) neurons are extensivelymodulated by cocaines inhibition of catecholaminereuptake at both the somatic and synaptic levels. Systemic cocaine binge administration in miceenhanced gamma-aminobutyric acid (GABA) releaseat the thalamic level that was correlated to abnormallyhigh levels of low-frequency oscillations at corticalelectroencephalography. Cocaine mediated local anesthetic-like effects, reducingaction potential frequency during whole-cellpatch-clamp recordings in TRN neurons. Multiple cocaine binge administration increased proteinlevels of T-type CaV3.1 and glutamate decarboxylaseon TRN-VB synapses. Long-lasting cocaine effects on GABAergic neurotransmissionmight be mediated by homeostatic compensatorymechanisms at TRN.