CAMP-Dependent protein kinase A activity modulates topiramate potentiation of GABA A receptors

Timothy A. Simeone, Karen S. Wilcox, H. Steve White

Research output: Contribution to journalArticle

8 Scopus citations

Abstract

Activation of cAMP-dependent protein kinase A (PKA) prevents inhibition of non-NMDA glutamate receptors by the anticonvulsant topiramate. Using two-electrode voltage-clamp techniques, we demonstrate that PKA activity also modulates topiramate potentiation of recombinant GABA A receptors expressed in Xenpus laevis oocytes. PKA activators, dibutyryl-cAMP and forskolin, attenuate topiramate potentiation, whereas the PKA inhibitor H-89 increases topiramate potentiation. Thus, endogenous PKA activity and receptor phosphorylation states may contribute to topiramate treatment efficacy.

Original languageEnglish (US)
Pages (from-to)176-179
Number of pages4
JournalEpilepsy Research
Volume96
Issue number1-2
DOIs
StatePublished - Sep 1 2011

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology

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