Reduced calcium binding protein immunoreactivity induced by electroconvulsive shock indicates neuronal hyperactivity, not neuronal death or deactivation

J. E. Kim, S. E. Kwak, D. S. Kim, M. H. Won, O. S. Kwon, S. Y. Choi, T. C. Kang

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

Calcium-binding proteins (CBPs), such as parvalbumin and calbindin D-28k, are useful markers of specific neuronal types in the CNS. In recent studies, expression of CBPs may be indicative of a deactivated neuronal state, particularly epilepsy. However, it is controversial whether altered expression of CBPs in the hippocampus practically indicate neuronal activity. Therefore, the present study was performed to investigate the extent of profiles of expression of CBPs in the rat hippocampus affected by several episodes induced by electroconvulsive shock. In the present study, following electroconvulsive shock expression of CBPs were reduced in the hippocampus in a stimulus-dependent manner, and recovered to the control level at 6 h after electroconvulsive shock. However, paired-pulse responses of the dentate gyrus were transiently impaired by electroconvulsive shock, and immediately normalized to baseline value. In addition, effects of electroconvulsive shock on expression of CBPs and paired-pulse responses were prevented by pretreatment of vigabatrin. These findings suggest that reduced expression of CBPs induced by seizure activity may be indicative of hyperactivity of CBP positive neurons, which is a practical consequence of the abnormal discharge, and that they may play an important role in regulating seizure activity.

Original languageEnglish
Pages (from-to)317-326
Number of pages10
JournalNeuroscience
Volume137
Issue number1
DOIs
StatePublished - 2006

Keywords

  • Calbindin D-28K
  • Electroconvulsive shock
  • Hippocampus
  • Parvalbumin
  • Rat

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