DECREASE IN SOMATOSTATIN-IMMUNOREACTIVE NEURONS IN THE RAT AMYGDALOIDCOMPLEX IN A KINDLING MODEL OF TEMPORAL-LOBE EPILEPSY

In human temporal lobe epilepsy, seizures can begin in the hippocampus , amygdala, or surrounding cortical areas. Histologically, the seizure -induced selective neuronal damage and synaptic reorganization are bes t documented in the hippocampus. Little information is available about the damage in the other temporal lobe structures, or whether the dist ribution of damage depends on the location of the primary seizure focu s. We used an amygdala-kindling model of temporal lobe epilepsy to stu dy whether seizures of amygdaloid origin cause damage to the amygdala and hippocampus. All rats experienced five class 5 generalized seizure s. Neuronal damage was assessed by counting the density of GABA-immuno reactive (GABA-ir) and somatostatin-immunoreactive (SOM-ir) neurons in the amygdala and hilus of the dentate gyrus six months after the last seizure. We found that the density of GABA-ir neurons did not differ from that in controls in the contralateral amygdala. The density of SO M-ir neurons was, however, decreased in the lateral (69% of neurons re maining, P < 0.01), basal (67% remaining, P < 0.05), and accessory bas al (68% remaining. P < 0.05) nuclei. In the hilus, the densities of GA BA-ir and SOM-ir neurons were similar to that in controls. According t o our data, a few seizures of amygdaloid origin may cause more severe damage to SOM-ir neurons in the amygdala than in the hilus. Such decre ase in SOM-ir neurons which form one subpopulation of GABAergic inhibi tory interneurons may increase the local excitability in the amygdala and, therefore, contribute to epileptogenesis. (C) 1997 Elsevier Scien ce B.V.