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Alteration in expression of G-protein-activated inward rectifier K+-channel subunits GIRK1 and GIRK2 in the rat brain following electroconvulsive shock.

Authors: Pei, Q  Lewis, L  Grahame-Smith, DG  Zetterstrom, TS 
Citation: Pei Q, etal., Neuroscience. 1999 May;90(2):621-7.
Pubmed: (View Article at PubMed) PMID:10215164

G-protein-activated inward rectifier potassium channels are coupled to a number of neurotransmitter receptors, including some monoamine receptors. In the present study we have investigated the effect of electroconvulsive shock on gene expression of the G-protein-activated inward rectifier potassium channel subunits G-protein-coupled inward rectifier K+-channel (GIRK1) and GIRK2 in the rat brain using in situ hybridization and immunocytochemistry. Acute electroconvulsive shock (a single shock) increased GIRK2 expression while causing a transient reduction of the messenger RNA abundance of GIRK1 in granule cells of the dentate gyrus. Chronic electroconvulsive shock (five shocks over 10 days) caused a larger increase in GIRK2 messenger RNA abundance, which was accompanied by an increase in GIRK2 immunoreactivity in the molecular layer of the dentate gyrus. Unlike for acute electroconvulsive shock, GIRK1 messenger RNA abundance in the dentate gyrus was significantly increased after chronic electroconvulsive shock. No significant alterations in GIRK1 and GIRK2 messenger RNA abundance were detected in the other brain regions studied, including the CA1 and CA3 subfields of the hippocampus, the frontal-parietal cortex and piriform cortex. The neuroanatomically specific changes in expression of the potassium channel subunits may directly influence neuronal excitability as well as the functions of G-protein-coupled neurotransmitter receptors.


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CRRD Object Information
CRRD ID: 2316513
Created: 2010-02-15
Species: All species
Last Modified: 2010-02-15
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.