DEPOLARIZATION OF NEURONS IN THE ISOLATED OLFACTORY CORTEX OF THE GUINEA-PIG BY GAMMA-AMINOBUTYRIC ACID

Effects of γ‐aminobutyric acid (GABA) on single neurones in slices of guinea‐pig olfactory cortex maintained in vitro were recorded with single intracellular microelectrodes. The average resting potential of 52 cells was — 75 mV and apparent input resistance ranged from 20 to 200 MQ. Superfusions of GABA over the slice invariably depolarized the neurones and reduced their input resistance. The minimum effective concentration was 50 to 200 um. The reversal potential for the depolarization produced by 0.1 mm GABA (Eg) was — 66 ± 2 mV. At concentrations >0.1 mm the reversal potential became progressively more positive (— 55 to −50mV). Reduction of external chloride, with isethionate as the substitute anion, increased the amplitude of the depolarization. GABA reduced the amplitude of the excitatory postsynaptic potential produced by lateral olfactory tract stimulation, and occluded or reversed the subsequent depolarizing recurrent inhibitory postsynaptic potential. Action potentials elicited by injection of depolarizing current or by focal antidromic stimulation were slowed and reduced in amplitude by GABA. The effects of GABA on membrane conductance (potency = 1) were duplicated by 3‐aminopro‐panesulphonic acid (potency = 20), j5‐alanine (0.5), 0‐amino‐w‐butyric acid (0.5), glycine (0.3) and L‐2,4‐diaminobutyric acid (0.2). For a given conductance change, 3‐aminopropanesulphonic acid, glycine and β‐alanine produced less depolarization than did GABA. It is concluded that the action of GABA on the neurones is compatible with a role in mediating recurrent postsynaptic inhibition. 1979 British Pharmacological Society