J. Tuunanen et al., DECREASE IN SOMATOSTATIN-IMMUNOREACTIVE NEURONS IN THE RAT AMYGDALOIDCOMPLEX IN A KINDLING MODEL OF TEMPORAL-LOBE EPILEPSY, Epilepsy research, 26(2), 1997, pp. 315-327
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.