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

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

Content Provider	Semantic Scholar
Author	Huber, Kimberly M. Mauk, Michael D. Kelly, Paul T.
Copyright Year	1995
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.
File Format	PDF HTM / HTML
DOI	10.1097/00001756-199506090-00013
PubMed reference number	7669987
Journal	Medline
Volume Number	6
Issue Number	9
Alternate Webpage(s)	http://clm.utexas.edu/mmlab/wp-content/uploads/2015/07/HuberMaukKelly95Neuroreport.pdf
Alternate Webpage(s)	https://doi.org/10.1097/00001756-199506090-00013
Journal	Neuroreport
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article

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