It is now well established that striatal lesions induce motor and cognitive
deficits in rats, and that grafts of embryonic striatal tissue can survive
, integrate into the lesioned host brain and alleviate the behavioural defi
cits in both motor and cognitive spheres. How? Since normal striatal functi
on is dependent upon it's integration within a connected cortical-subcortic
al neuronal circuitry, and the deficits following striatal damage appear to
reflect a "disconnexion" syndrome, the observation of recovery suggests th
at the grafts re-establish a connected circuitry within the host brain. Evi
dence to corroborate or refute this hypothesis, in comparison with a less-s
pecific mechanism (or mechanisms) of recovery, is considered, including ana
tomical, electrophysiological and neurochemical demonstrations of functiona
l circuit reconstruction in the host brain by striatal tissue transplants.