Effect of amygdala kindling on GABA neurons: histochemical and biochemical detection of GABA-T activity.

Although a number of studies have been focused on the role of 7-aminobutyric acid (GABA) in the kindling model of epilepsy (see Review, e.g., 5 ) , the functional significance of GABA neurons is still controversial. In the present study, we attempted to find possible alterations in the central GABA neurons of amygdala-kindled rats by means of histochemical and biochemical techniques. Although GABA-transaminase (GABA-T) , the catabolyzing enzyme of GABA, has been considered not a reliable marker for GABAergic neurons, the new pharmacohistochemical procedure using a specific and irreversible inhibitor appears to visualize presumptive GABAergic perikarya.4 The present histochemical data demonstrated an extensive loss of GABA-T intensive neuronal perikarya in the kindled amygdala, and the result was confirmed by a biochemical measurement of GABA-T activity. Seventy male Sprague-Dawley rats were used. Under pentobarbital anesthesia, bipolar electrodes were stereotaxically implanted in the left amygdala. At least one week after surgery, electrical stimulations ( 1 -sec train of 60 Hz biphasic pulses) were delivered until sustaining five consecutive full seizures. For controls intact and sham-operated rats were used. Seven to 10 days after the final stimula-