Seizure-induced damage to somatostatin-immunoreactive neurons in the rat hippocampus is regulated by fimbria-fornix transection
Abstract
In both experimental and human temporal lobe epilepsy, seizures cause loss of hilar somatostatin-immunoreactive (SOM-ir) neurons and sprouting of mossy fibers. To investigate whether in rats these alterations are modulated by hippocampal input projections, we transected the fimbria-fornix or the perforant pathway bilaterally 2 days after seizures induced by systemic administration of kainic acid (9 mg/kg, i.p.). Two months later, the number of SOM-ir neurons in the hilus was counted and mossy fiber sprouting in the supragranular area and in the inner molecular layer was analyzed. In seizured rats with sham-operation, 50% of the hilar SOM-ir neurons were left in the septal end of the hippocampus and only 16% remained in the temporal end. In seizured rats with transection of the fimbria-fornix, the number of hilar SOM-ir neurons in the septal end of the hippocampus did not differ from that in controls (98% of SOM-ir neurons left). However, the temporal end was severely damaged (41% of SOM-ir neurons left). In seizured rats with transection of the perforant pathway, 61% of the hilar SOM-ir neurons were left in the septal end and 51% in the temporal end of the hippocampus. Mossy fiber sprouting was evident throughout the septotempo...Continue Reading
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