Elevated endogenous GABA level correlates with decreased fMRI signals in the rat brain during acute inhibition of GABA transaminase
Version of Record online: 23 DEC 2004
Copyright © 2004 Wiley-Liss, Inc.
Journal of Neuroscience Research
Volume 79, Issue 3, pages 383–391, 1 February 2005
How to Cite
Chen, Z., Silva, A. C., Yang, J. and Shen, J. (2005), Elevated endogenous GABA level correlates with decreased fMRI signals in the rat brain during acute inhibition of GABA transaminase. J. Neurosci. Res., 79: 383–391. doi: 10.1002/jnr.20364
- Issue online: 12 JAN 2005
- Version of Record online: 23 DEC 2004
- Manuscript Accepted: 11 OCT 2004
- Manuscript Revised: 8 OCT 2004
- Manuscript Received: 6 JUL 2004
- functional imaging;
- in vivo spectroscopy;
Vigabatrin and gabaculine, both highly specific inhibitors of GABA (γ-aminobutyric acid) transaminase, cause significant elevation of endogenous GABA levels in brain. The time course of GABA concentration after acute GABA transaminase inhibition was measured quantitatively in the α-chloralose-anesthetized rat brain using in vivo selective homonuclear polarization transfer spectroscopy. The blood oxygenation level-dependent (BOLD) effect in functional magnetic resonance imaging (fMRI) has been considered to be coupled tightly to neuronal activation via the metabolic demand of associated glutamate transport. Correlated with the rise in endogenous GABA level after vigabatrin or gabaculine treatment, the intensity of BOLD-weighted fMRI signals in rat somatosensory cortex during forepaw stimulation was found to be reduced significantly. These results are consistent with previous findings that inhibition of GABA transaminase leads to augmented GABA release and potentiation of GABAergic inhibition. © 2004 Wiley-Liss, Inc.