Abstract
The effects of inhibitory (γ-aminobutyric acid (GABA) and glycine) and excitatory ( l-glutamate and dl-homocysteate, DLH) amino acids on the excitability of respiratory bulbospinal neurons were studied in decerebrate, paralyzed, bilaterally vagotomized, artificially ventilated cats. Unit activities were recorded extracellularly in the medulla in both the ventrolateral portion of the nucleus tractus solitarius and the para-ambigual region in the vicinity of the nucleus ambiguus (dorsal and ventral respiratory groups, respectively). All neurons were bulbospinal since they could be antidromically activated by electrical stimuli to the spinal cord. We used variations in antidromic latency (ADL) as a measure of changes in excitability of the soma. All neurons exhibited variations in ADL related to the respiratory cycle, being shortest (minimum ADL) during neural activity and longest (maximum ADL) in the silent period. Neurons whose discharge frequencies fell during application of putative inhibitory amino acids showed an increase of minimum ADL compared to control, indicating hyperpolarization. Minimum ADL, in some cells, became shorter during application of excitatory amino acids, indicating depolarization; in others, mechanisms secondary to increased neuronal firing likely obscured their effects. The transient maximum ADL usually present at the onset of the silent period was increased by excitatory amino acids and, in some units, was reduced or eliminated by inhibitory amino acids. These effects are discussed in terms of a modulation by synaptic inputs and neurotransmitters of the cumulative afterhyperpolarization which follows bursts of action potentials.
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