INHIBITORY POSTSYNAPTIC CURRENTS AND THE EFFECTS OF GABA ON VISUALLY IDENTIFIED SACRAL PARASYMPATHETIC PREGANGLIONIC NEURONS IN NEONATAL RATS

1. The actions of gamma-aminobutyric acid (GABA) on sacral parasympath etic preganglionic (SPP) neurons were examined in slice preparations u sing the whole eel patch-clamp technique. 2. Inhibitory postsynaptic c urrents (IPSCs), which were evoked by focal electrical stimulation, we re recorded from SPP neurons in the presence of 6-cyano-7-nitroquinoxa line-2,3-dione (CNQX), a glutamate receptor antagonist. The IPSCs were substantially reduced by strychnine (1 mu M), a glycine receptor anta gonist. The remaining IPSCs were completely blocked by bicuculline (20 mu M), a GABA(A) receptor antagonist. The mean peak amplitude of bicu culline-sensitive, GABAergic currents recorded at -60 mV was 53.6 +/- 10.9%, mean +/- SD (n = 8), of that of the total IPSCs. The GABAergic currents were reversed in polarity at about -30 mV, near the Cl- equil ibrium potential. 3. GABA (5-50 mu M) induced inward currents in SPP n eurons with symmetrical internal and external Cl- concentrations. This response was completely blocked by 100 mu M bicuculline. Muscimol (2- 8 mu M), a GABA(A) agonist, mimicked the GABA-induced responses, where as a GABA(B) receptor agonist, baclofen (20-200 mu M), produced respon ses in only a few cells. The GABA-induced currents reversed their pola rity at similar to 0 mV, near the Cl- equilibrium potential. When the internal Cl- concentration was reduced, the reversal potential was shi fted according to the Nernst equation for Cl-. 4. GABA-induced current s exhibited an outward ''hump'' between -35 and 15 mV. This voltage ra nge coincided with that at which a depolarization-induced inward whole cell current was elicited. Both the GABA-induced outward hump and the depolarization-induced inward current disappeared when external Ca2or Ba2+ was replaced with Mn2+ 5. Ca2+ currents induced by a depolariz ing pulse to 0 mV from a holding potential of -80 mV were reversibly s uppressed by GABA. This effect was mimicked by baclofen but not by mus cimol. The GABA(B) receptor antagonist, 2-OH-saclofen (500 mu M), redu ced the inhibitory actions of GABA or baclofen. 6. The degree of inhib ition of Ca2+ currents by GABA was enhanced with depolarization up to similar to 0 mV but reduced when the cell was further depolarized. 7. It is concluded that GABA(A) receptors, the predominant type of GABA r eceptor operating in SPP neurons, mediate IPSCs to the almost same ext ent as glycine receptors, and that activation of a minor population of GABA(B) receptors can diminish Ca2+ currents significantly.