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

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.

Ingår i:Journal of neurophysiology: American Physiological Society103:1, s. 441-4451522-15980022-3077

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