Mechanisms of modulation of AMPA-induced Na+-activated K+ current by mGluR1

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Fältnamn	Indikatorer	Metadata
000		02073naa a2200253 4500
001		oai:prod.swepub.kib.ki.se:119898890
003		SwePub
008		240811s2010 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
024	7	a http://kipublications.ki.se/Default.aspx?queryparsed=id:1198988902 URI
024	7	a https://doi.org/10.1152/jn.00584.20092 DOI
040		a (SwePub)ki
041		a engb eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Nanou, E4 aut
245	1 0	a Mechanisms of modulation of AMPA-induced Na+-activated K+ current by mGluR1
264	1	b American Physiological Society,c 2010
520		a Na+-activated K+ (KNa) channels can be activated by Na+ influx via ionotropic receptors and play a role in shaping synaptic transmission. In expression systems, KNa channels are modulated by G protein–coupled receptors, but such a modulation has not been shown for the native channels. In this study, we examined whether KNa channels coupled to AMPA receptors are modulated by metabotropic glutamate receptors (mGluRs) in lamprey spinal cord neurons. Activation of mGluR1 strongly inhibited the AMPA-induced KNa current. However, when intracellular Ca2+ was chelated with 1,2-bis(2-aminophenoxy)ethane- N,N,N′, N′-tetraacetic acid (BAPTA), the KNa current was enhanced by mGluR1. Activation of protein kinase C (PKC) mimicked the inhibitory effect of mGluR1 on the KNa current. Blockade of PKC prevented the mGluR1-induced inhibition of the KNa current, but did not affect the enhancement of the current seen in BAPTA. Together these results suggest that mGluR1 can differentially modulate AMPA-induced KNa current in a Ca2+- and PKC-dependent manner.
700	1	a El Manira, Au Karolinska Institutet4 aut
710	2	a Karolinska Institutet4 org
773	0	t Journal of neurophysiologyd : American Physiological Societyg 103:1, s. 441-445q 103:1<441-445x 1522-1598x 0022-3077
856	4 8	u http://kipublications.ki.se/Default.aspx?queryparsed=id:119898890
856	4 8	u https://doi.org/10.1152/jn.00584.2009

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Av författaren/redakt...: Nanou, E; El Manira, A

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Av lärosätet: Karolinska Institutet

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