We studied the effects of transient forebrain ischemia in vivo on long-term enhancement of dopamine (DA) release from rat striatal slices. One hour after the high-frequency tetanic stimulation (HFTS) or l-glutamate (10-6 M) application in Mg2+-free medium to striatal slices, the high concentration of KCl (high K+)-evoked DA release was measured. Tetanic stimulation or l-glutamate application significantly potentiated the high-K+-evoked DA release. When striatal slices were prepared from rats exposed to 3 min of ischemia followed by 24-h survival, the enhancement of DA release by HFTS was unaffected by ischemia. In contrast, the enhancement of DA release by HFTS was impaired in rats exposed to 5 min or 10 min of ischemia. In addition, high K+-evoked DA release per se was significantly impaired by 10 min of ischemia. The enhancement of DA release elicited by pretreatment with l-glutamate was also impaired in the rats exposed to 5 min of ischemia. When striatal slices were prepared from rats exposed to 5 min of ischemia with 7-day survival, the enhancement of DA release by HFTS was still impaired. The present results indicate that the neuronal mechanisms of the enhancement of DA release may be more sensitive to impairement from short periods of ischemia. Furthermore, the results suggest that an impairment of long-term enhancement of DA release by ischemia may be related the dysfunction of motor performance in rats exposed to ischemia.
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