Taurine Improves Congestive Functions in a Mouse Model of Fragile X Syndrome
Increased seizure susceptibility is a feature of the mouse model for fragile X that has parallels in the hyperarousal and prevalence of seizures in the fragile X syndrome. Our investigation of the basis for the increased seizure susceptibility of the fragile X mouse indicated a reduction in GABAA receptor expression and increased expression of glutamic acid decarboxylase (GAD), the enzyme responsible for GABA synthesis. Taurine-fed mice also show these GABAergic alterations. However, unlike fragile X mice, taurine-fed mice show a significant increase in memory acquisition and retention. This discordance implies that there may be divergent events downstream of the biochemical changes in the GABAergic system in these two mouse models. To investigate the divergence of these two models we fed taurine to fragile X mice. Our preliminary data shows that taurine supplementation to fragile X mice resulted in a significant improvement in acquisition of a passive avoidance task. Since taurine is an agonist for GABAA receptor, we suggest that chronic activation of GABAA receptors and the ensuing alterations in the GABAergic system may have beneficial effects in ameliorating the learning deficits characteristic of the fragile X syndrome.
KeywordsPassive Avoidance Glutamic Acid Decarboxylase Dark Compartment GABAergic System Passive Avoidance Task
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