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XB-ART-44787
Epilepsy Res 2011 Sep 01;961-2:176-9. doi: 10.1016/j.eplepsyres.2011.05.009.
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cAMP-dependent protein kinase A activity modulates topiramate potentiation of GABA(A) receptors.

Simeone TA, Wilcox KS, White HS.


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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.

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Genes referenced: camp