Silencing the vagus nerve produces homeostatic changes at second order nucleus tractus solitarius synapses

Abstract

Many diseases, pathologies and medical treatments alter vagal nerve activity, but the underlying central nervous system changes caused by these treatments are not well understood. My study was designed to test how silencing action potential activity in the vagus nerve of rats affects synaptic plasticity at second order nucleus tractus solitarius (NTS) synapses. At least seven days following unilateral vagotomy, in vitro horizontal brainstem slices containing the NTS were prepared for whole cell patch clamp recording. Vagotomy caused a homeostatic increase in evoked excitatory postsynaptic current (evEPSC) amplitudes and a decrease in the frequency of spontaneous EPSCs (spEPSCs). These results were dramatically altered by including the GABAA receptor antagonist, bicuculline (BIC), in the recording bath. In order to test whether the results observed following vagotomy were due to the loss of impulse activity, rather than the influence of inflammatory or other injury-induced factors, I implanted rats for six to eight days with a cuff containing the sodium channel blocker tetrodotoxin (TTX). After six to eight days, I removed the brainstem and prepared in vitro horizontal NTS slices. Similar to vagotomy, TTX treatment caused a homeostatic increase in evEPSC amplitudes and a decrease in the frequency of spEPSCs. No alterations to passive or active postsynaptic membrane properties following TTX treatment or vagotomy observed, nor were spEPSC amplitudes changed. These results suggest that silencing vagal impulse activity causes a homeostatic increase in synaptic efficacy at monosynaptic NTS synapses.