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) |
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Pages (from-to) | 176-179 |
Number of pages | 4 |
Journal | Epilepsy Research |
Volume | 96 |
Issue number | 1-2 |
DOIs | |
State | Published - Sep 2011 |
All Science Journal Classification (ASJC) codes
- Neurology
- Clinical Neurology