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 Citations (Scopus)

Abstract

We have examined the requirement for protein kinase activity in long-term potentiation (LTP) induced by activation of voltage-dependent Ca2+ channels (VDCCs) in hippocampal slices. We previously demonstrated that LTP induced by application of the K+ channel blocker tetraethylammonium (TEA-LTP) consisted of two distinct components, an NMDA receptor-dependent component and 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
StatePublished - 1995

Fingerprint

Long-Term Potentiation
Protein Kinases
Calcium-Calmodulin-Dependent Protein Kinase Type 2
KN 62
Tetraethylammonium
N-Methylaspartate
Protein Kinase Inhibitors
N-Methyl-D-Aspartate Receptors
Enzymes

Keywords

  • Calcium
  • Calmodulin/dependent
  • Long term potentiation
  • NMDA receptor
  • Protein kinase II
  • Voltage-dependent calcium channel

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

LTP induced by activation of voltage-dependent Ca2+ channels requires protein kinase activity. / Huber, K. M.; Mauk, M. D.; Kelly, P. T.

In: NeuroReport, Vol. 6, No. 9, 1995, p. 1281-1284.

Research output: Contribution to journalArticle

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AU - Mauk, M. D.

AU - Kelly, P. T.

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N2 - We have examined the requirement for protein kinase activity in long-term potentiation (LTP) induced by activation of voltage-dependent Ca2+ channels (VDCCs) in hippocampal slices. We previously demonstrated that LTP induced by application of the K+ channel blocker tetraethylammonium (TEA-LTP) consisted of two distinct components, an NMDA receptor-dependent component and 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.

AB - We have examined the requirement for protein kinase activity in long-term potentiation (LTP) induced by activation of voltage-dependent Ca2+ channels (VDCCs) in hippocampal slices. We previously demonstrated that LTP induced by application of the K+ channel blocker tetraethylammonium (TEA-LTP) consisted of two distinct components, an NMDA receptor-dependent component and 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.

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