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 |
|---|---|
| Pages (from-to) | 176-179 |
| Number of pages | 4 |
| Journal | Epilepsy Research |
| Volume | 96 |
| Issue number | 1-2 |
| DOIs | |
| Publication status | Published - Sep 2011 |
Fingerprint
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 journal › Article