Vigabatrin enhances promoted release of GABA in neonatal rat optic nerve

Epilepsy Research
J M YeeJ D Kocsis

Abstract

Vigabatrin (gamma-vinyl GABA) is an antiepileptic drug and blocks GABA transaminase activity resulting in elevations in cellular GABA levels in the brain. Nipecotic acid (NPA) promotes release of GABA from neonatal optic nerve astrocytes, resulting in a bicuculline-sensitive depolarization of the optic nerve axons. The NPA-induced depolarization of vigabatrin-treated rats (100 mg/kg, i.p.) more than doubled, suggesting an elevation in free GABA levels; the GABA transporter inhibitor, NO-711 reduced the depolarization. These results are consistent with the known ability of vigabatrin to block the GABA degradation enzyme GABA-transaminase, suggesting that vigabatrin elevates astrocytic GABA levels, thereby favoring greater release of GABA through the GABA transporter.

References

Dec 1, 1980·Journal of Neurochemistry·J A Moscowitz, R W Cutler
Mar 14, 1994·Neuroscience Letters·J D Kocsis, O Honmou

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Citations

Oct 26, 1999·Epilepsia·M J McLean
Nov 24, 1999·Epilepsia·J M Rho, R Sankar
Apr 14, 2010·Epilepsia·Aphrodite DracopoulosO Carter Snead
Sep 13, 2008·Progress in Neurobiology·María Cecilia AnguloEtienne Audinat
Sep 13, 2008·Journal of Neurochemistry·Tanja VihavainenTimo Petteri Piepponen
Sep 19, 2003·Journal of Neurophysiology·Nikolai AxmacherRaphael Ritz
Sep 3, 2002·Journal of Neurophysiology·L Barakat, A Bordey

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