Glutamate decarboxylase and Gamma amino transeferase levels in different regions of rat brain on the onset of Electroshock induced convulsions

The imbalance in the pools of excitatory or inhibitory neurotransmitters at their nerve endings causes depolarization or hyperpolarisation of the postsynaptic membrane. The heightened neuronal activity of the brain results in convulsions. Since Glutamate and ?-Aminobutyric acid (GABA) play an important metabolic role, quantitative changes in the content of this amino acid during altered neuronal activity may be possible. Although different convulsants such as drugs or electroshock may cause convulsions by different mechanisms, the basic change is an increase in neuronal firing. In order to understand the probable changes in the neurotransmitter pools of glutamate and GABA during convulsions, the enzymes involved in the production, liberation and disposal of glutamate and GABA, during pre, post and convulsions caused by electroshock have been studied. Convulsions were induced in white albino rats weighing 150-200 grams with convulsometer of “Techno” India using corneal electrodes. The animals were grouped into four. Group I served as control, whereas Group II-IV was subjected to electroconvulsions. The animals were sacrificed and the cerebral cortex, cerebellum and brainstem were separated from the brain. The tissue homogenates were used to estimate the enzymes such as GAD and GABA-T. The results showed that the activity of Glutamate decarboxylase (GAD) decreases significantly (p<0.001) in all the three regions of the brain in all the three phases. The activity of ?-Aminobutyric acid transferase (GABA-T) decreases significantly (p<0.001) in all the three brain regions in all the three phases of convulsions. Therefore, it is suggested that the concomitant changes of GAD activity and GABA concentration is probably an important factor in the onset of convulsions.