title: GABAB receptors modulate a tetanus-induced sustained potentiation of monosynaptic inhibitory transmission in the rat nucleus tractus solitarii in vitro.
abstract: Whole-cell recordings were made in the nucleus tractus solitarii (NTS) in transverse brainstem slices from rats. Monosynaptic GABAA-receptor-mediated inhibitory postsynaptic currents (IPSCs) or potentials (IPSPs) were evoked (0.1-0.2 Hz) by electrical stimulation within and medial to the tractus solitarius in the presence of the ionotropic glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM) or 6,7-dinitroquinoxaline-2,3-dione (DNQX; 10 microM) and D-amino-5-phosphonopentanoic acid (APV; 50 microM). A brief period of tetanic stimulation (20 Hz, 2 s) resulted in posttetanic (< 5 min, 69 of 73 recordings) and sustained potentiation (> 15 min, 31 of 73 recordings) of the IPSP/Cs. Sustained potentiation was not due to alterations in the reversal potential of IPSP/Cs. Both pre- and post-tetanus IPSP/Cs were completely blocked by the GABAA antagonist bicuculline (10 microM). Postsynaptic responses to pressure ejection of the GABAA-receptor agonist muscimol were unaltered in cells displaying sustained potentiation. Sustained potentiation of IPSP/Cs could be induced by tetanus in the presence of either metabotropic glutamate receptor antagonists or bicuculline. However, sustained potentiation could not be induced in the presence of the GABAB-receptor antagonists 2-OH-saclofen (400 microM) or CGP35348 (3-amino-propyl-(diethoxymethyl)phosphinic acid, 100 microM), although a subsequent tetanus following washout induced sustained potentiation. Posttetanic potentiation was unaffected by GABAB-receptor antagonists. These data suggest that neuronal or terminal excitability of GABAergic interneurons in the NTS is enhanced following brief periods of increased frequency of activation in vitro. This novel phenomenon within the rat medulla may be involved in the temporal modulation of autonomic reflex sensitivity observed during certain behavioral states, such as the defense reaction.
authors.affiliation: Department of Physiology, Royal Free Hospital School of Medicine, London, UK.
authors.forename: P A
authors.initials: PA
authors.lastname: Brooks
authors.forename: S R
authors.initials: SR
authors.lastname: Glaum
mesh_terms: D000818:Animals; D004558:Electric Stimulation; D066298:In Vitro Techniques; D017774:Long-Term Potentiation / Q000187:drug effects; D008564:Membrane Potentials / Q000187:drug effects*; D018408:Patch-Clamp Techniques; D051381:Rats; D011919:Rats, Inbred Strains; D018080:Receptors, GABA-B / Q000187:drug effects*; D017552:Solitary Nucleus / Q000187:drug effects*; D009435:Synaptic Transmission / Q000187:drug effects*; D013742:Tetanus / Q000378:metabolism; D013997:Time Factors
chemical_list: D018080:Receptors, GABA-B