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Endogenous GABAA receptor‐mediated attenuation of hypoglossal motorneuronal discharge activity in vivo

Inspiratory hypoglossal motor neurons (IHMNs) mediate excitatory drive to upper airway muscles to maintain airway patency during sleep and stimulated breathing. IHMNs in decerebrate dogs receive excitatory glutamatergic and serotonergic drive input. This current study examined the role of endogenous GABAAergic input on IHMN discharge patterns in decerebrate, vagotomized, paralyzed, and mechanically ventilated dogs. The GABAA receptor antagonist bicuculline (BIC, 200 μM) was picoejected onto extracellularly‐recorded single IHMNs using multibarrel micropipettes. Spike‐triggered averaging or serotonergic responsiveness was used to identify IHMNs. The discharge patterns were analyzed via cycle‐triggered histograms triggered at the onset of the phrenic neurogram. Dose‐rates were increased until no further excitation was observed. Only phasic inspiratory activity was affected by BIC. At peak BIC dose‐rates, the peak frequency of the ramp‐like discharge patterns of 11 IHMNs increased by 46 ± 6%. The slope and y‐intercept of the relationship between the control and BIC patterns were 1.34 ± 0.06 and 6 ± 2 Hz, respectively. These data suggest that IHMNs are subject to gain modulation via tonic GABAergic inhibition during hypercapnic hyperoxia. These effects appear to be smaller than those encountered in inspiratory bulbospinal neurons.