The modulation of baroreceptor inputs to NTS neurons by GABA receptor subtypes was investigated in pentobarbital anesthetized, paralyzed and artificially ventilated rats. Aortic nerve (AN) evoked discharge was classified as monosynaptic (MS; second of two stimuli separated by 5ms evoked discharge; minimal onset latency variability) or polysynaptic (PS). The effects of iontophoresis of GABA (2mM) or the GABAn agonist baclofen (lOmM) using currents of 10,20&40nA were examined on single pulse AN evoked discharge and spontaneous discharge. GABA inhibited MS AN inputs at currents of 20&40nA (p<.05, n=7) and inhibited PS inputs at all 3 currents (p<.01, n=9). GABA was more potent at inhibiting PS compared to MS inputs (p<.05). GABA increased AN evoked action potential amplitude suggesting membrane potential hyperpolarization. In contrast to GABA, baclofen did not inhibit MS AN inputs at any current (p=. 26, n=3) but inhibited PS inputs at all 3 currents (p<. 05, n=3). Baclofen appeared to induce much smaller increases in action potential amplitude compared to GABA, GABA and baclofen inhibited the spontaneous discharge of AN evoked cells at all 3 currents (p<.01, n=5 MS & 3 PS for GABA and n=3 MS for baclofen). These results suggest that GABAA receptors produce post-synaptic hyperpolarization and inhibition of MS and PS AN evoked and spontaneous discharge in NTS neurons. Pre-synaptic mechanisms also appear to be involved in the inhibition of PS AN inputs by GAB AB receptors.
|Publication status||Published - 1 Dec 1996|