STATUS EPILEPTICUS CAUSES SELECTIVE REGIONAL DAMAGE AND LOSS OF GABAERGIC NEURONS IN THE RAT AMYGDALOID COMPLEX

In human epilepsy, the amygdala is often a primary focus for seizures. To analyse the status epilepticus-induced alterations in the amygdalo id circuitries which may later underlie epileptogenesis, we studied th e amygdaloid damage in kainic acid and perforant pathway stimulation m odels of status epilepticus in the rat. We also studied the damage to inhibitory GABAergic neurons. in both models, the medial division of t he lateral nucleus, the parvicellular division of the basal nucleus an d portions of the anterior cortical and medial nuclei were damaged. In the kainate model, where the seizure activity was more severe, the ac cessory basal nucleus, amygdalohippocampal area, posterior cortical nu cleus and periamygdaloid cortex were also damaged. Two weeks after kai nate-induced seizures, 56% of the GABA-immunoreactive neurons remained in the lateral nucleus (P < 0.05) and 25% in the basal nucleus (P < 0 .01). Further analysis showed that one subpopulation of damaged GABAer gic neurons was immunoreactive for somatostatin (48% remaining in the lateral nucleus, P < 0.01; 33% in the basal nucleus, P < 0.01). In the perforant pathway stimulation model, the damage to somatostatin neuro ns was milder. According to our data, the initial insult, such as stat us epilepticus, selectively damages amygdaloid nuclei. The loss of inh ibition may underlie the spontaneous generation of seizures and epilep togenesis. On the other hand, many amygdaloid output nuclei (magnocell ular and intermediate division of the basal nucleus, the central nucle us) remained relatively undamaged, providing pathways for seizure spre ad and generation of seizure-related behavioural manifestations such a s motor convulsions and fear response.