Metabotropic-mediated kainate receptor regulation of IsAHP and excitability in pyramidal cells
Metabotropic-mediated kainate receptor regulation of IsAHP and excitability in pyramidal cells
Kainate receptors (KARs) on CA1 pyramidal cells make no detectable contribution to EPSCs. We report that these receptors have a metabotropic function, as shown previously for CA1 interneurons. Brief kainate exposure caused long-lasting inhibition of a postspike potassium current (IsAHP) in CA1 pyramidal cells. The pharmacological profile was independent of AMPA receptors or the GluR5 subunit, indicating a possible role for the GluR6 subunit. KAR inhibition of IsAHP did not require ionotropic action or network activity, but was blocked by the inhibitor of pertussis toxin-sensitive G proteins, N-ethylmaleimide (NEM), or the PKC inhibitor calphostin C. These data suggest how KARs, putatively containing GluR6, directly increase excitability of CA1 pyramidal cells and help explain the propensity for seizure activity following KAR activation.
107-114
Melyan, Z.
698dea51-50d8-4429-87f7-86d2dca3227e
Wheal, H.V.
50ba5833-9920-407a-a48a-1fe917534b74
Lancaster, B.
6491671f-ae25-4974-849d-3b74f6bed448
2002
Melyan, Z.
698dea51-50d8-4429-87f7-86d2dca3227e
Wheal, H.V.
50ba5833-9920-407a-a48a-1fe917534b74
Lancaster, B.
6491671f-ae25-4974-849d-3b74f6bed448
Melyan, Z., Wheal, H.V. and Lancaster, B.
(2002)
Metabotropic-mediated kainate receptor regulation of IsAHP and excitability in pyramidal cells.
Neuron, 34 (1), .
(doi:10.1016/S0896-6273(02)00624-4).
Abstract
Kainate receptors (KARs) on CA1 pyramidal cells make no detectable contribution to EPSCs. We report that these receptors have a metabotropic function, as shown previously for CA1 interneurons. Brief kainate exposure caused long-lasting inhibition of a postspike potassium current (IsAHP) in CA1 pyramidal cells. The pharmacological profile was independent of AMPA receptors or the GluR5 subunit, indicating a possible role for the GluR6 subunit. KAR inhibition of IsAHP did not require ionotropic action or network activity, but was blocked by the inhibitor of pertussis toxin-sensitive G proteins, N-ethylmaleimide (NEM), or the PKC inhibitor calphostin C. These data suggest how KARs, putatively containing GluR6, directly increase excitability of CA1 pyramidal cells and help explain the propensity for seizure activity following KAR activation.
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Submitted date: 10 August 2001
Published date: 2002
Identifiers
Local EPrints ID: 35561
URI: http://eprints.soton.ac.uk/id/eprint/35561
ISSN: 0896-6273
PURE UUID: e09c2347-ad56-4175-96f4-6805a1b53239
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Date deposited: 26 Jan 2007
Last modified: 15 Mar 2024 07:52
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Author:
Z. Melyan
Author:
H.V. Wheal
Author:
B. Lancaster
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