Neurogenesis of gasping does not require inhibitory transmission using GABA(A) or glycine receptors

Abstract

We evaluated the hypothesis that the neurogenesis of gasping is not dependent upon inhibitory synaptic transmission involving GABA(A) or glycine receptors. Activity of the phrenic nerve was recorded in a perfused juvenile rat preparation. The pattern of phrenic activity was altered from eupnea to gasping in severe hypoxia or ischaemia. To block GABA(A) receptors, bicuculline or picrotoxin was administered. Strychnine was used to block transmission by glycine. Following administrations of bicuculline, picrotoxin or strychnine, the eupneic rhythm was greatly distorted whereas the decrementing pattern of the gasp was maintained. At high concentrations of these antagonists, the frequency of gasps was increased and the peak height of gasps fell. We conclude that the neurogenesis of gasping is not dependent upon fast, chloride-mediated inhibitory synaptic transmission.