Tamoxifen, a chloride channel blocker, reduces glutamate and aspartate release from the ischemic cerebral cortex.
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.
Phillis
J W
JW
Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
Song
D
D
O'Regan
M H
MH
D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism*; D002540:Cerebral Cortex / Q000098:blood supply / Q000737:chemistry / Q000378:metabolism; D018118:Chloride Channels / Q000037:antagonists & inhibitors; D004965:Estrogen Antagonists / Q000494:pharmacology*; D018698:Glutamic Acid / Q000378:metabolism*; D002546:Ischemic Attack, Transient / Q000188:drug therapy / Q000378:metabolism*; D008297:Male; D018696:Neuroprotective Agents / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013629:Tamoxifen / Q000494:pharmacology*
D018118:Chloride Channels; D004965:Estrogen Antagonists; D018696:Neuroprotective Agents; D013629:Tamoxifen; D001224:Aspartic Acid; D018698:Glutamic Acid