Shifts of cortical d.c. potential induced by application of gamma-aminobutyric acid in rats in vivo.

Abstract

Generally, increases in cortical activity go in parallel with negative shifts and decreases with positive shifts of cortical d.c. potentials. The aim of the present investigation was to test the effects of the inhibitory transmitter gamma-aminobutyric acid (GABA) and of GABA receptor agonists on cortical d.c. potentials. Concomitant changes of local pH were measured to get first insights as to the mechanisms of the evoked d.c. changes. The experiments were carried out on anesthetized and artificially ventilated rats. d.c. potentials were recorded at a cortical depth of about 1000 microm by glass microelectrodes. Extracellular pH was measured by ion-selective microelectrodes. GABA (0.1 mol/l), the GABA(A) receptor agonist muscimol (0.1 mmol/l) and the GABA(B) receptor agonist baclofen (0.1 mmol/l) were microejected by pressure pulses at a distance of 20-40 microm from the recording electrode. GABA evoked positive d.c. shifts with low pressure ejection and long application times. With increasing pressure the positive d.c. shifts were initially superimposed by negative ones. The GABA(A) receptor agonist muscimol elicited negative and the GABA(B) receptor agonist baclofen positive displacements of the d.c. potential independent of application time or pressure. The negative d.c. shifts induced by GABA and muscimol were associated with an extracellular alkalization of up to 0.1 pH units. The findings led one to assume (1) that the negative d.c. shift after GABA application was due to a neuronal depolarization and to an increase in excitation via local alkalization and (2) that the positive d.c. shift mirrored neuronal hyperpolarization.