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• W2347149245 startingPage "391" @default.
• W2347149245 abstract "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, Ih and IA, 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 IA and Ih 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 IA and Ih were present in subsets of GABA+ and GABA- neurons. Interestingly, GABA+ neurons with Ih were more responsive to afferent stimulation than inhibitory neurons devoid of these currents, whereas GABA- neurons with IA were more subject to inhibitory modulation. These results suggest that the voltage-gated channels underlying IA and Ih play an important role in modulating rNST output through a circuit of feedforward inhibition." @default.
• W2347149245 created "2016-06-24" @default.
• W2347149245 creator A5015887937 @default.
• W2347149245 creator A5020845132 @default.
• W2347149245 creator A5088992606 @default.
• W2347149245 date "2016-08-01" @default.
• W2347149245 modified "2023-09-26" @default.
• W2347149245 title "Inhibitory modulation of optogenetically identified neuron subtypes in the rostral solitary nucleus" @default.
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• W2347149245 doi "https://doi.org/10.1152/jn.00168.2016" @default.
• W2347149245 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4969383" @default.
• W2347149245 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27146980" @default.
• W2347149245 hasPublicationYear "2016" @default.
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