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Inhibition is presumed to play an important role in gustatory processing in the rostral nucleus of the solitary tract (rNST). One source of inhibition, GABA, is abundant within the nucleus and comes both from local, intrasolitary sources and from outside the nucleus. In addition to the receptor-mediated effects of GABA on rNST neurons, the hyperpolarization-sensitive currents, I h  and I A , have the potential to further modulate afferent signals. To elucidate the effects of GABAergic modulation on solitary tract (ST)-evoked responses in phenotypically defined rNST neurons and to define the presence of I A  and I h  in the same cells, we combined in vitro recording and optogenetics in a transgenic mouse model. This mouse expresses channelrhodopsin 2 (ChR2) in GAD65-expressing GABAergic neurons throughout the rNST. GABA positive (GABA+) neurons differed from GABA negative (GABA−) neurons in their response to membrane depolarization and ST stimulation. GABA+ neurons had lower thresholds to direct membrane depolarization compared with GABA− neurons, but GABA− neurons responded more faithfully to ST stimulation. Both I A  and I h  were present in subsets of GABA+ and GABA− neurons. Interestingly, GABA+ neurons with I h  were more responsive to afferent stimulation than inhibitory neurons devoid of these currents, whereas GABA− neurons with I A  were more subject to inhibitory modulation. These results suggest that the voltage-gated channels underlying I A  and I h  play an important role in modulating rNST output through a circuit of feedforward inhibition.

Inhibitory modulation of optogenetically identified neuron subtypes in the rostral solitary nucleus