2Department of Neurosurgery, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada.
3,7,8Department of Molecular Biology and Genetics, Boğaziçi University, Istanbul, Turkey
4,5,9Department of Neurosurgery, Cerrahpasa Medical Faculty, İstanbul University, Istanbul, Turkey.
6Department of Histology and Embryology, Medical Faculty, Marmara University, Istanbul, Turkey. AIM: Hyperpolarization-activated cyclic nucleotide-gated (HCN or h-channel) channels mediate hyperpolarization-activating currents in the hippocampus and neocortex. The aim of this study is to present prenatal h-channel gene expressions (HCN1 and HCN2; HCN1-Entrez-Gene ID: 84390; HCN2- Entrez Gene ID: 114244) in dysplastic hippocampal pyramidal neurons induced by in utero irradiation in rats.
MATERIALS and METHODS: Time-pregnant Wistar albino rats were irradiated and the dysplastic hippocampus in their 2 month-old litters was studied. Gene expression was studied by RNA extraction and polymerase chain reaction methods.
RESULTS: None of the rats showed seizure activity. mRNA levels of HCN1 and HCN2 genes were decreased especially in the CA1 and CA3 pyramidal neurons in the hippocampi of experimental rats; however, the differences were not significant compared to controls. In CA2, mRNA levels of both genes were increased and this rise did not reach significant level. The CA4 sub-region showed a different pattern of expression: HCN1 increased but HCN2 decreased insignificantly compared to controls.
CONCLUSION: Our results demonstrated that dysplastic neurons showed decreased levels of mRNA expression of HCN1 and HCN2 genes, in particularly CA1 and CA3 pyramidal neurons. The rationale for how these changes contribute to epileptogenesis in dysplastic tissues still requires further studies.
Keywords : Dysplasia, HCN1, HCN2, Gene expression, Hippocampal sclerosis, Temporal lobe epilepsy