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The purpose of this study was to elucidate the role of the GABAergic system in the medullary reticular formation (MRF) in the control of swallowing. In acutely decerebrated cats (n = 12), swallowing was induced by electrical stimulation (0.3-6 V at 10-20 Hz for 10-20 s every minute) applied to the superior laryngeal nerve (SLN). The stimulus intensity was adjusted so that swallowing was induced two or four times during the period of the stimulation. Bicuculline, a GABA(A) receptor antagonist, was then injected (0.10-0.15 microl, 5 mM) into the MRF through a stereotaxically placed glass micropipette. In a total of 62 injections, 19 injections (30.6%) increased the frequency of SLN-induced swallowing when it was injected into the lateral part of the MRF corresponding to the nucleus reticularis parvocellularis (NRPv). In eight of the effective injections (42.1%) which increased the frequency of SLN-induced swallowing, SLN stimulation also induced coughing. With two injections, stimulation of the SLN-induced coughing but not facilitation of swallowing. On the other hand, an injection of 0.10-0.15 microl of 5 mM muscimol, a GABA(A) receptor agonist, into the NRPv decreased the frequency of SLN-induced swallowing. These results suggest that the NRPv neurons which are responsible for evoking swallowing are under the tonic inhibitory control of the GABAergic system.

We identified a potential novel site of action for nicotine (NIC) since (a) systemic injection of NIC led to a dose-dependent decrease in the amplitude of the sleep state-dependent, vertex-recorded, P13 midlatency auditory evoked potential (generated by the reticular activating system, RAS), (b) localized injections of a nicotinic receptor antagonist into the pedunculopontine nucleus (PPN, the cholinergic arm of the RAS) blocked the effects of systemic NIC on the P13 potential (a measure of level of arousal), and (c) localized injection of a nicotinic receptor agonist into the PPN also led to a decrease in the amplitude of the P13 potential, an effect blocked by PPN injection of a nicotinic receptor antagonist. There were minor changes in the manifestation of the startle response (SR) at the concentrations used; however, NIC did decrease the hippocampal N40 potential, although its effects were not affected by antagonist or agonist injections into the PPN. These results suggest a potential mechanism underlying the anxiolytic effects of NIC-suppression of the cholinergic arm of the RAS.