Abstract

Neurons within the parabrachial (PB) complex appear to play a key role in controlling breathing frequency. Densely labeled GABA‐immunoreactive varicosities have been observed throughout the PB and the Kölliker‐Fuse (KF) nuclei of rats, however, the role of GABAergic control of PRG neurons is inadequately understood. To characterize GABAergic inhibition in the control of PRG discharge frequency (Fn) patterns, we analyzed the effects of microejected GABA‐A receptor antagonists bicuculline and picrotoxin on PRG neuronal activity in a decerebrate, vagotomized, ventilated and paralyzed canine model. Histograms (CTHs) triggered from the phrenic neurogram were used to quantify neuronal unit activity. Both antagonists produced marked increases in Fn (>80%) either alone or combined (sequentially ejected) in 80‐90% of PRG neurons. Activity throughout the cycle of phase spanning PRG neurons was increased and phasic portions of Fn showed gain modulation. Effects of both antagonists appear to be qualitatively and quantitatively similar. The results show that most PRG neurons are under strong endogenous GABAergic inhibition that attenuates their activity and is expected to markedly impact phase‐timing.Grant Funding Source: Supported by VA Medical Research Funds I01 BX000721‐01

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