GABA and IA Independently Regulate rNST Responses to Afferent Input

Abstract

Taste responses in the rostral nucleus of the solitary tract (rNST) influence motivated ingestive behavior via ascending pathways, and consummatory reflex behavior via local, brainstem connections. Modifications to the afferent signal within the rNST include changes in gain (the overall rate of neuron activity) and changes in gustatory tuning (the degree to which individual neurons respond to divergent gustatory qualities). These alterations of the sensory signal derive from both synaptic interactions within the nucleus and the constitutive cellular membrane properties of rNST neurons. GABA neurons are well represented within the rNST, as is expression of KV4.3, a channel for a rapidly inactivating outward K+ current (IA). GABAergic synapses suppress rNST responses to afferent input and previous studies showed that this suppression is greater in cells expressing IA, suggesting a possible interaction. Here, we examine the potential interaction between GABAergic inhibition and IA channels in a series of patch clamp experiments. Optogenetic release of GABA suppressed rNST responses to afferent (electrical) stimulation and this effect was greater in cells with IA, confirming an earlier report. We further observed that the composite inhibitory postsynaptic potential was larger in IA positive cells, suggesting one mechanism for the greater afferent suppression. Blocking IA with the channel blocker AmmTX3, enhanced the response to afferent stimulation, suggesting a suppressive role for this channel in regulating afferent input at rest. However, pharmacologic blockade of IA did not suppress GABAergic inhibition, indicating that IA and GABA independently regulate excitatory afferent input.