Journal
JOURNAL OF NEUROPHYSIOLOGY
Volume 103, Issue 1, Pages 441-445Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/jn.00584.2009
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Funding
- Swedish Research Council
- Soderberg Foundation
- European Commission [Health-F2-2007-201144]
- Wings for Life Foundation
- Karolinska Institutet
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Nanou E, El Manira A. Mechanisms of modulation of AMPA-induced Na+-activated K+ current by mGluR1. J Neurophysiol 103: 441-445, 2010. First published November 4, 2009; doi: 10.1152/jn.00584.2009. Na+-activated K+ (K-Na) channels can be activated by Na+ influx via ionotropic receptors and play a role in shaping synaptic transmission. In expression systems, K-Na 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 K-Na 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 K-Na current. However, when intracellular Ca2+ was chelated with 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid (BAPTA), the K-Na current was enhanced by mGluR1. Activation of protein kinase C (PKC) mimicked the inhibitory effect of mGluR1 on the K-Na current. Blockade of PKC prevented the mGluR1-induced inhibition of the K-Na current, but did not affect the enhancement of the current seen in BAPTA. Together these results suggest that mGluR1 can differentially modulate AMPA-induced K-Na current in a Ca2+- and PKC-dependent manner.
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