Effects of L-glutamate and GABA on the response of expiratory neurons to mechanical loads

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Abstract
Expiratory neurons in the area of the nucleus retroambigualis were studied in anesthetized cats to determine their responsiveness to the iontophoretic application of the putative neurotransmiters, glutamate and gamma‐aminobutyric acid (GABA). Previous studies with glutamate and GABA revealed that these two substances were very effective in modulating the spontaneous activity of phasic medullary respiratory neurons. Mechanical loading of expiration, both resistive and elastic, was employed to test whether the presence of these transmitter substances altered the sensitivity of the expiratory cell to its volume related vagal input. Expiratory unit activity analysis included: spikes/burst, burst duration, and average firing rate. Addition of mechanical loads on expiration caused consistent increases in all parameters monitored. Iontophoretically applied glutamate (x̄ = 65 nA) resulted in modest increases in all parameters. When mechanical loads were applied in the presence of a sustained level of glutamate the effects were additive. The general shape of the firing profile observed with loading remained essentially unchanged. Application of GABA (x̄ = 46 nA) resulted in a significant decrease in the parameters monitored. However, as long as phasic activity remained, loads applied in the presence of GABA produced approximately the same absolute change as they did during control. Some cells exposed to high concentrations of GABA lost their phasic activity. This study suggests that either the synaptically activated receptors are not affected by glutamate or that these particular sites are not accessible via iontophoretic application. GABA depressed the activity of the cells in a graded fashion, but in modest concentrations did not interfere with the overall effectiveness of the vagally mediated input.