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This Article Full Text Full Text (PDF) All Versions of this Article: 579/2/363    most recent jphysiol.2006.122051v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Grabauskas, G. Articles by Wheal, H. V. Search for Related Content PubMed PubMed Citation Articles by Grabauskas, G. Articles by Wheal, H. V. Related Collections Neuroscience

¹ School of Biological Sciences, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, UK
² Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, UK

Hippocampal pyramidal neurones display a Ca²⁺-dependent K⁺ current responsible for the slow afterhyperpolarization (I_sAHP), a prominent regulator of excitability. There is considerable transmitter convergence onto I_sAHP but little information about the interplay between the kinase-based transduction mechanisms underlying transmitter action. We have added to existing information about the role of protein kinase C (PKC) in kainate receptor actions by demonstrating that direct postsynaptic activation of PKC with either 1-oleoyl-2-acethylsn-glycerol (OAG) or indolactam is sufficient to inhibit I_sAHP. The physiological correlate of this action – activation of PKC by kainate receptors – requires G_i/o proteins. The cAMP/PKA system is well documented to subserve the actions of monoamine transmitters. We have found an additional role for the cAMP/PKA system as a requirement for kainate receptor-mediated inhibition of I_sAHP. Inhibition of adenylyl cyclase with dideoxyadenosine or PKA with either H89 or RpcAMPs blocked kainate receptor-mediated actions but did not prevent the actions of direct PKC activation with either OAG or indolactam. We therefore propose that the PKA requirement is upstream from the actions of PKC. We additionally report a downstream link in the form of increased mitogen-activated protein (MAP) kinase activity, which may explain the long duration of metabotropic actions of kainate receptors on I_sAHP.

(Received 3 October 2006; accepted after revision 5 December 2006; first published online 7 December 2006)
Corresponding author H. V. Wheal: School of Biological Sciences, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, UK. Email: h.v.wheal{at}soton.ac.uk

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