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

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

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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
Pages (from-to)176-179
Number of pages4
JournalEpilepsy Research
Volume96
Issue number1-2
DOIs
Publication statusPublished - Sep 2011

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All Science Journal Classification (ASJC) codes

  • Clinical Neurology
  • Neurology

Cite this

CAMP-Dependent protein kinase A activity modulates topiramate potentiation of GABA A receptors. / Simeone, Timothy; Wilcox, Karen S.; White, H. Steve.

In: Epilepsy Research, Vol. 96, No. 1-2, 09.2011, p. 176-179.

Research output: Contribution to journalArticle