Seizure-induced damage to somatostatin-immunoreactive neurons in the rat hippocampus is regulated by fimbria-fornix transection.

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 septotemporal axis of the hippocampus in all seizured rats. Our results suggest that in the septal end of the hippocampus the severity of neuronal damage in the hilus is modulated by mechanism(s) that are dependent on the afferent pathways entering the hippocampus via the fimbria-fornix. Transection of the fimbria-fornix, however, does not significantly modulate the severity or the target regions of seizure-induced sprouting of mossy fibers.