Dopaminergic neurotransmission triggers ischemia-induced hyperactivity in Mongolian gerbils

It is recognized that sustained ischemia-induced hyperactivity is related t o abnormalities in dopamine function. However, it is unclear that dopaminer gic neurotransmission triggers such ischemia-induced hyperactivity. Therefo re, the relationship between dopaminergic neurotransmission and ischemia-in duced hyperactivity was investigated in an animal model using Mongolian ger bils. When haloperidol 2 mg/kg was administered i.p. 30 min after ischemia, the ischemia-induced hyperactivity at 24 h after ischemia was blocked. Gen eral behavior was similar to that of sham-operated animals. Haloperidol at doses of 0.1 and 0.2 mg/kg had no effect on locomotor activity in sham-oper ated animals and decreased ischemia-induced hyperactivity when the drug was administered 24 h after ischemia; these doses did not have any effect on i schemia-induced hyperactivity when the drug was administered 30 min after i schemia. On the other hand, when the animal was confined to a small, restri ctive cage for the 24 h period immediately following ischemic injury, locom otor activity at 24 h after ischemia increased. Such behavior also increase d in animals when they were returned to their original more permissive cage s immediately after ischemia. It is conceivable that the decrease in the le vel of activity was not related to ischemia-induced hyperactivity. These da ta suggested that the inhibition of ischemia-induced hyperactivity can be i nduced by complete blockage of dopaminergic receptors immediately after isc hemia.