Alterations in hyperpolarization-activated cyclic nucleotidegated cation channel (HCN) expression in the hippocampus following pilocarpine-induced status epilepticus

• Main Author: Yun-Jung Oh, Jongju Na, Ji-Heon Jeong, Dae-Kyoon Park, Kyung-Ho Park, Jeong-Sik Ko & Duk-Soo Kim*
• Format: Article
• Language: English
• Published: Korean Society for Biochemistry and Molecular Biology 2012-11-01
• Series: BMB Reports
• Subjects: Epilepsy; HCN channels; Hippocampus; Immunohistochemistry; Status epilepticus
• Online Access: http://www.jbmb.or.kr/jbmb/pdf.php?data=MTMwMTIyMTZAcGRmX3JhaW50cmFjZV9sZWV5c0AlNUI0NS0xMSU1RDEyMTEyOTEzNTBfJTI4NjM1LTY0MCUyOUJNQl8xMi0wOTEucGRm

To understand the effects of HCN as potential mediators in thepathogenesis of epilepsy that evoke long-term impairedexcitability; the present study was designed to elucidate whetherthe alterations of HCN expression induced by status epilepticus(SE) is responsible for epileptogenesis. Although HCN1 immunoreactivitywas observed in the hippocampus, its immunoreactivitieswere enhanced at 12 hrs following SE. Although, HCN1immunoreactivities were reduced in all the hippocampi at 2weeks, a re-increase in the expression at 2-3 months followingSE was observed. In contrast to HCN1, HCN 4 expressions wereun-changed, although HCN2 immunoreactive neurons exhibitedsome changes following SE. Taken together, our findings suggestthat altered expressions of HCN1 following SE may be mainlyinvolved in the imbalances of neurotransmissions to hippocampalcircuits; thus, it is proposed that HCN1 may play animportant role in the epileptogenic period as a compensatoryresponse.