Consequences of intrastriatally administrated FeCl3 and 6-OHDA without and after transient cerebral oligemia on behaviour and navigation

6-OHDA (6 or 8 µg) unilaterally applied into the ventrolateral striatum induces neurotoxic effects which lead to unilateral hyperactivity triggering contralateral turning and rotations after apomorphine administration. Treatment with alpha-tocopherol prevents the hypersensitive reaction. The sensitivity of the cerebral tissue to apomorphine following 6-OHDA treatment is enhanced when 7.5 µg FeCl3 is coadministered with 6-OHDA. Only when the combination of 6-OHDA and FeCl3 is administered the escape latency to find a hidden platform in a water maze-test increased as measured 12 weeks later. The night activity of such treated animals was markedly reduced. Remarkable effects of unilaterally applied FeCl3 (0.06–1.5 ug) were observed in old rats, and in rats after transient cerebral oligemia. Apomorphine treatment to such animals induced rotations. It is possible, therefore, that mild to moderate transient or permanent local oxygen deficits together with iron cause progressive damage to vulnerable cerebral tissue. Such an effect would be comparable to the neurotoxicity of 6-OHDA possibly involve free radicals and lipid peroxidation.