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.
All Science Journal Classification (ASJC) codes
- Clinical Neurology
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.
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