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 language | English (US) |
|---|---|
| Pages (from-to) | 176-179 |
| Number of pages | 4 |
| Journal | Epilepsy Research |
| Volume | 96 |
| Issue number | 1-2 |
| DOIs | |
| State | Published - Sep 1 2011 |
All Science Journal Classification (ASJC) codes
- Neurology
- Clinical Neurology
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Simeone, T. A., Wilcox, K. S., & White, H. S. (2011). CAMP-Dependent protein kinase A activity modulates topiramate potentiation of GABA A receptors. Epilepsy Research, 96(1-2), 176-179. https://doi.org/10.1016/j.eplepsyres.2011.05.009