Journal
JOURNAL OF NEUROSCIENCE
Volume 24, Issue 19, Pages 4530-4534Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.5356-03.2004
Keywords
calphostin C; hippocampus; kainic acid; potassium channels; protein kinase C; pyramidal cells; kainate receptor
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Funding
- Wellcome Trust [069189] Funding Source: Medline
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Prolonged modification of intrinsic neuronal excitability is gaining prominence as an activity-dependent form of plasticity. Here we describe a potential synaptic initiation mechanism for these changes in which release of the transmitter glutamate acts on kainate receptors to regulate the postspike slow afterhyperpolarization (sAHP). This action of synaptically released glutamate was occluded by previous kainate application. Furthermore, inhibition of glutamate uptake enhanced the effects of synaptic activation. Glutamate-mediated kainate receptor inhibition of sAHP current (I(sAHP)) was blocked by the PKC inhibitor calphostin C, confirming the requirement for a metabotropic signaling cascade. These data describe a new physiological function for glutamate release: activation of metabotropic kainate receptors, which control directly the excitability of pyramidal cells and probably contribute to prolonged excitability changes.
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