Ethanol affects the respiratory control network through more than GABA receptors

Abstract

Central nervous system networks that drive oscillatory activity rely on inhibitory amino acids like GABA for rhythm generation. Application of GABA to an intact but isolated ventilatory‐control network elicits an overall reduction in respiratory rhythm. In isolated bullfrog tadpole brainstem preparations the reduction in respiratory nerve output is both a decline in lung burst frequency and an abolition of gill‐associated neuroventilation. Ethanol is a GABA‐mimetic, and the ventilatory reduction exhibited during acute ethanol exposure has been associated with GABA‐meditated pathways. Chronic ethanol exposure has been found to attenuate responses to subsequent exposure to GABA and ethanol in the tadpole brainstem preparation. Despite these correlations between GABA and ethanol, preliminary experiments using acute ethanol application failed to reduce tadpole gill‐associated neuroventilation concomitant with a clear decrease in lung burst frequency. This suggests the effect of ethanol on respiratory rhythm generation is not exclusive to GABA‐mediated neurotransmission or, alternatively, that the role of GABA in the amphibian respiratory control network is more complex than previously speculated.