Epilepsy Research
Volume 29, Issue 3 , Pages 195-200, February 1998

Vigabatrin enhances promoted release of GABA in neonatal rat optic nerve

Department of Neurology, Yale University School of Medicine and Neuroscience Research Center (127A), VA Medical Center, West Haven, CT 06516, USA

Received 11 February 1997; received in revised form 1 June 1997; accepted 15 September 1997.

Abstract 

Vigabatrin (γ-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.

Keywords:  Vigabatrin, GABA, Epilepsy, GABA transaminase

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PII: S0920-1211(97)00086-7

Epilepsy Research
Volume 29, Issue 3 , Pages 195-200, February 1998

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