Chronic methamphetamine administration inhibits cerebral ischemia-induced hyperactivity in Mongolian gerbils.

The effect of single and chronic methamphetamine (MAP) administration on ischemia-induced hyperactivity was investigated and the mechanism of ischemia-induced hyperactivity was discussed. Ischemia-induced hyperactivity was recognized 3 h after ischemia. However, ischemia-induced hyperactivity at 1 day after ischemia was inhibited when MAP, in a dose of 10 mg/kg, was administered for 7 days and withdrawn for 7 days. It was reported that MAP treatment caused an irreversible decrease in the number of dopamine (DA) uptake sites. In addition to this, monoamine oxidase and the uptake of DA into the nerve terminals are disturbed by cerebral ischemia. Therefore, a lot of DA release happened during and immediately after ischemia, and a marked down-regulation of DA receptor occurred 24 h after ischemia in MAP-injected group. It is conceivable that the DA receptor, especially the presynaptic DA uptake site, is related to the occurrence of ischemia-induced hyperactivity. Further studies appear to be necessary to clarify acceptor susceptibility when neurotransmitters are normalized after transient ischemia.