Decreased glutamate release during hypothyroidism may contribute to protection in cerebral ischemia.

Hypothyroidism protects the brain from the effects of transient forebrain ischemia in gerbils. The mechanism for this protection is not fully understood. In this study we looked at the release of glutamate during ischemia in gerbils exposed to surgical hypothyroidism (n = 7), chemical hypothyroidism (n = 8), and surgical hypothyroidism thyroxine-treated (n = 3) and compared them to control euthyroid animals (n = 8). The duration of ischemia was 10 min. Glutamate release was measured with in vivo microdialysis. Microdialysis analysis began 2 h after the placement of the probes (to stabilize the baseline) and collections were obtained in 10-min samples. During ischemia, there was an increase in the release of glutamate that returned to the baseline within 20 min following the insult. In animals made hypothyroid surgically and chemically, the extent of glutamate release was significantly lower than that in the controls. The release of glutamate in the surgically hypothyroid thyroxine-treated animals was similar to that in controls. The attenuated glutamate release could be a mechanism of protection during ischemia in hypothyroid gerbils.