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Metabotropic regulation of intrinsic excitability by synaptic activation of kainate receptors

Metabotropic regulation of intrinsic excitability by synaptic activation of kainate receptors
Metabotropic regulation of intrinsic excitability by synaptic activation of kainate receptors
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 (IsAHP) 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.
calphostin C, hippocampus, kainic acid, potassium channels, protein kinase C, pyramidal cells, kainate receptor
0270-6474
4530-4534
Melyan, Z.
698dea51-50d8-4429-87f7-86d2dca3227e
Lancaster, B.
6491671f-ae25-4974-849d-3b74f6bed448
Wheal, H.V.
50ba5833-9920-407a-a48a-1fe917534b74
Melyan, Z.
698dea51-50d8-4429-87f7-86d2dca3227e
Lancaster, B.
6491671f-ae25-4974-849d-3b74f6bed448
Wheal, H.V.
50ba5833-9920-407a-a48a-1fe917534b74

Melyan, Z., Lancaster, B. and Wheal, H.V. (2004) Metabotropic regulation of intrinsic excitability by synaptic activation of kainate receptors. Journal of Neuroscience, 24 (19), 4530-4534. (doi:10.1523/JNEUROSCI.5356-03.2004).

Record type: Article

Abstract

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 (IsAHP) 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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Submitted date: 4 December 2003
Published date: 12 May 2004
Keywords: calphostin C, hippocampus, kainic acid, potassium channels, protein kinase C, pyramidal cells, kainate receptor

Identifiers

Local EPrints ID: 35563
URI: http://eprints.soton.ac.uk/id/eprint/35563
ISSN: 0270-6474
PURE UUID: 4bc7d1b3-6884-4ce3-ae53-0527bbfded6e

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Date deposited: 19 May 2006
Last modified: 08 Jan 2022 15:54

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Contributors

Author: Z. Melyan
Author: B. Lancaster
Author: H.V. Wheal

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