Cx36 in the mouse hippocampus during and after pilocarpine-induced status epilepticus.

Gap junctions play an important role in the synchronization activity of coupled cells. Hippocampal inhibitory interneurons are involved in epileptogenesis and seizure activity, and express gap junction protein connexin (Cx) 36. Cx36 is also localized in the axons (mossy fibers) of granule cells in the dentate gyrus. While it has been documented that Cx36 is involved in epileptogenesis, there are still controversies regarding the expression levels of Cx36 at different developmental stages of human and animal models of epileptogenesis. In this study, the expression of Cx36 was investigated in the mouse hippocampus at 1 h, 4 h during pilocarpine-induced status epilepticus (PISE) and 1 week, 2 months after PISE. We found that Cx36 was down-regulated in neurons at different time points during and after PISE, whereas it was increased significantly in the stratum lucidum of CA3 area at 2 months after PISE. Double immunofluorescence indicated that Cx36 was localized in parvalbumin (PV) immunopositive interneuron in CA1 area and in mossy fibers and their terminals in the stratum lucidum of CA3 area. It suggests that decreased expression of Cx36 in interneurons may be related to less effective inhibitory control of excitatory activity of hippocampal principal neurons. However, the increased Cx36 immunopositive product in mossy fibers at the chronic stage after PISE may enhance the contacts between granule cells in the dentate gyrus and pyramidal neurons in CA3 area. The two different changes of Cx36 may be implicated in the epileptogenesis.

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