LTP induced by activation of voltage-dependent Ca2+ channels requires protein kinase activity

K. M. Huber, M. D. Mauk, P. T. Kelly

Research output: Contribution to journalArticle

12 Scopus citations

Abstract

A VDCC-dependent component. The results herein demonstrate that both the NMDA and VDCC-dependent components of TEA-LTP are blocked by K-252a, a broad spectrum protein kinase inhibitor. Furthermore, VDCC-dependent TEA-LTP is attenuated by KN-62, a specific inhibitor of Ca2+/calmodulin dependent protein kinase II (CaM-KII). These results demonstrate that LTP induced by VDCC activation requires protein kinase activity and suggest that different routes of postsynaptic Ca2+ influx activate protein kinases to trigger the induction of LTP but that these enzyme systems may be contained in different cell compartments.

Original languageEnglish (US)
Pages (from-to)1281-1284
Number of pages4
JournalNeuroReport
Volume6
Issue number9
DOIs
StatePublished - Jun 1995

Keywords

  • Calcium/Calmodulin-Dependent protein kinase II
  • Long term potentiation
  • NMDA receptor
  • Voltage-Dependent calcium channel

ASJC Scopus subject areas

  • Neuroscience(all)

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