Premium
Melatonin, vitamin E, and estrogen reduce damage induced by kainic acid in the hippocampus: potassium‐stimulated GABA release
Author(s) -
Ortiz Genaro G.,
SánchezRuiz Mayra Y.,
Tan DunXian,
Reiter Russel J.,
BenítezKing Gloria,
BeasZárate Carlos
Publication year - 2001
Publication title -
journal of pineal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 131
eISSN - 1600-079X
pISSN - 0742-3098
DOI - 10.1034/j.1600-079x.2001.310109.x
Subject(s) - melatonin , kainic acid , medicine , endocrinology , estrogen , neuroprotection , chemistry , kainate receptor , biology , glutamate receptor , receptor , ampa receptor
Melatonin, vitamin E and estrogen have been shown to exert neuroprotective effects against kainic acid (KA)‐induced damage in the hippocampus. The aim of the present study was to examine the changes in potassium‐evoked γ‐aminobutyric acid (GABA) release in the hippocampus of KA‐treated rats and to test the possible protective effects of melatonin, vitamin E or estrogen. Following the treatment of mice with KA, a marked reduction in potassium‐evoked [ 3 H]GABA release was observed. Melatonin or estrogen prevented the reduction in potassium‐evoked GABA release due to kainate administration. Vitamin E also exhibited some protective effect, but it was less than that provided by melatonin or estrogen. Melatonin, estrogen and, to a lesser extent, vitamin E reduce the physiological toxicity of KA. Since KA is believed to cause neuronal alterations via oxidative processes, it is assumed that the free radical scavenging and oxidative properties of melatonin, estrogen and vitamin E account for the protective effects of these agents.