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Tamoxifen, a chloride channel blocker, reduces glutamate and aspartate release from the ischemic cerebral cortex
J W Phillis1, D Song, M H O'Regan
1Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
The effects of the anti-estrogen, anion channel blocker, tamoxifen on amino acid release from the ischemic rat cerebral cortex was investigated using a cortical cup technique. Tamoxifen (20 microM in artificial cerebrospinal fluid), applied topically, inhibited the ischemia-evoked efflux of aspartate, glutamate, taurine and phosphoethanolamine. Reductions in the ischemia-evoked levels of these amino acids suggest that tamoxifen may attenuate chloride-related osmotic cell swelling and the associated regulatory volume decrease (RVD) release of amino acids.
The effects of the anti-estrogen, anion channel blocker, tamoxifen on amino acid release from the ischemic rat cerebral cortex was investigated using a cortical cup technique. Tamoxifen (20 microM in artificial cerebrospinal fluid), applied topically, inhibited the ischemia-evoked efflux of aspartate, glutamate, taurine and phosphoethanolamine. Reductions in the ischemia-evoked levels of these amino acids suggest that tamoxifen may attenuate chloride-related osmotic cell swelling and the associated regulatory volume decrease (RVD) release of amino acids.