Blockade of glycine receptors modifies temporal and spectral characteristics of phrenic nerve discharge in urethane‐anesthetized adult rat in vivo

Abstract

The neuronal mechanisms that underlie fast oscillatory rhythms in inspiratory‐related discharges are poorly understood; however, accumulating evidence suggests that fast synaptic inhibition may be amongst the mechanisms participating. In support of this idea, recent work from our laboratory in the urethane‐anesthetized adult rat preparation has shown that blockade of GABAA receptors modulates both the power and timing of spectral activity in phrenic nerve bursts. The role of glycine‐mediated synaptic inhibition requires clarification. Therefore, we examined the effects of glycine receptor antagonism, using cumulative increasing doses strychnine hydrochloride (STR; 0.2–10 mg/kg, iv), on phrenic nerve discharge in urethane‐anesthetized vagotomized adult rats (n=5). STR significantly decreased TI (from 325±43 to 208±24 ms; P=0.007) and TE (from 965±88 to 878±88 ms; P=0.031), resulting in an ~17% increase in burst frequency (P<0.004). STR also increased power of the MFO (by 123±61%) and HFO (by 83±65%) spectral peaks albeit this increase was not significant. Inspiratory network complexity (quantified by approximate entropy), however, was significantly reduced from 0.709±0.016 to 0.602±0.0198 (p=0.004). These findings suggest that glycine‐mediated synaptic inhibition may contribute to timing and spectral activity inherent in phrenic discharges in vivo. Supported by NS045321 and NS049310