No abstract

The rate of synthesis of γ‐aminobutyric acid (GABA) in the cortex, hippocampus and striatum of rat brain was assessed by measuring the linear rate of accumulation of GABA following injection of amino‐oxyacetic acid (AOAA). Five min after a single electrically induced seizure there was a rise in GABA content in these brain regions and an almost total inhibition of the rate of synthesis. Five min after seizure induced by the inhalant convulsant flurothyl there was no rise in GABA content in these brain regions but a similar marked degree of inhibition of GABA synthesis. Two hours after the convulsion the rate of GABA synthesis had returned to control values in all three brain regions. A single convulsion did not alter the glutamic acid decarboxylase activity in these brain regions either in the absence or presence of added co‐factor (pyridoxal phosphate). Evidence for an inhibition of GABA release following a convulsion which may be associated with the inhibition of GABA synthesis is presented in the following paper.

1 Following electroconvulsive shock (ECS) administration daily for 10 days there was an increase (35 %) in 5-hydroxytryptamine2 (5-HT2) receptor number in rat frontal cortex 24 h after the last ECS, compared with handled controls. A similar increase was seen after intermittent ECS administration (5 ECS over 10 days) given during halothane anaesthesia, compared with halothane-treated controls. The dissociation constant was also increased at this time. A single ECS had no effect. 2 Treatment of rats with pentylenetetrazol, p-chlorophenylalanine or a-methyl p-tyrosine during the intermittent ECS administration abolished the increase in 5-HT2 receptor binding. 3 Since enhanced 5-HT-mediated behavioural responses are seen after repeated ECS but not when the ECS is given with the drug treatments outlined above, it is suggested that ECS-induced enhancement of 5-HT-mediated behaviour results from an increase in 5-HT2 receptor number.

A method is described for the measurement of the K+‐evoked release of endogenous γ‐aminobutyric acid (GABA) from slices of rat cortex, hippocampus and striatum. In tissue prepared 30 min following an electroconvulsive shock, K+‐evoked GABA release (above basal release) was inhibited by 45% in cortex, 50% in hippocampus and 75% in striatum. A similar inhibition of release was observed with slices prepared from rats in which a convulsion had been induced by flurothyl. There was no change in spontaneous (basal) release following either procedure. An inhibition of K+‐evoked endogenous GABA release was also seen in tissue prepared 4 min postictally but not 2 h after the seizure. No difference was observed in the release of [3H]‐GABA from preloaded cortical slices prepared from rats given a single electroconvulsive shock. It is proposed that a convulsion results in an inhibition of GABA release and that this inhibition may in turn inhibit GABA synthesis as described in the preceding paper. It is also proposed that changes in the endogenous releasable pool of GABA may not be detected by preloading slices with [3H]‐GABA.