Acute reduction of neuronal RNA binding Elavl2 protein and Gap43 mRNA in mouse hippocampus after kainic acid treatment.
Activity-dependent gene regulation in neurons has been hypothesized to be under transcriptional control and to include dramatic increases in immediate early genes (IEGs) after neuronal activity. In addition, several reports have focused on post-transcriptional regulation, which could be mediated by neuronal post-transcriptional regulators, including RNA binding proteins (RNABPs). One such protein family is the neuronal Elavls (nElavls; Elavl2, Elavl3, and Elavl4), whose members are widely expressed in peripheral and central nervous system. Previous reports showed that Elavl3 and 4 are up-regulated following repeated stimulation such as during cocaine administration, a seizure, or a spatial discrimination task. In this study, we focused on Elavl2, a candidate gene for schizophrenia and studied its role in neuronal activity. First we found that Elavl2 has a cell-type specific expression pattern that is highly expressed in hippocampal CA3 pyramidal neurons and hilar interneurons using Elavl2 specific antibody. Second, unexpectedly, we discovered that the Elavl2 protein level in the hippocampus was acutely down-regulated for 3 h after a kainic acid (KA)-induced seizure in the hippocampal CA3 region. In addition, level of Gap43 mRNA, a target mRNA of Elavl2 is decreased 12 h after KA treatment, thus suggesting the involvement of Elavl2 in activity-dependent RNA regulation.
Department of Physiology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan.
Takafumi
T
Ohtsuka
Department of Physiology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan; Division of Neurobiology and Anatomy, Graduate School of Medical and Dental Sciences, Niigata University, 757, Ichibancho, Asahimachidori, Chuo-ku, Niigata-shi, Niigata, Japan. Electronic address: myano@med.niigata-u.ac.jp.
Masato
M
Yano
Department of Physiology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan. Electronic address: hidokano@a2.keio.jp.
Hideyuki
H
Okano
D000818:Animals; D056654:CA3 Region, Hippocampal / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D000067777:ELAV-Like Protein 2 / Q000032:analysis / Q000378:metabolism*; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology*; D019922:GAP-43 Protein / Q000235:genetics*; D005786:Gene Expression Regulation / Q000187:drug effects; D007395:Interneurons / Q000166:cytology / Q000378:metabolism; D007608:Kainic Acid / Q000494:pharmacology*; D008297:Male; D051379:Mice; D017966:Pyramidal Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics* / Q000378:metabolism; D012640:Seizures / Q000139:chemically induced
D000067777:ELAV-Like Protein 2; D018690:Excitatory Amino Acid Agonists; D019922:GAP-43 Protein; D012333:RNA, Messenger; D007608:Kainic Acid
Elavl2; Neuronal activity; Post-transcriptional control; RNA binding protein