CHANGES IN THE MITOCHONDRIAL ENZYME-ACTIVITY IN STRIATAL PROJECTION AREAS AFTER UNILATERAL EXCITOTOXIC STRIATAL LESIONS - PARTIAL RESTORATION BY EMBRYONIC STRIATAL TRANSPLANTS
N. Nakao et al., CHANGES IN THE MITOCHONDRIAL ENZYME-ACTIVITY IN STRIATAL PROJECTION AREAS AFTER UNILATERAL EXCITOTOXIC STRIATAL LESIONS - PARTIAL RESTORATION BY EMBRYONIC STRIATAL TRANSPLANTS, Experimental neurology, 153(2), 1998, pp. 268-276
It is well established that the activity of cytochrome oxidase (CO), a
mitochondrial enzyme, reflects the long-term, steady-state levels of
neuronal activity The present study investigated the long-term effects
of unilateral striatal lesions induced by quinolinic acid on CO activ
ity in primary striatal targets, including the globus pallidus (GP), e
ntopeduncular nucleus (EP), and substantia nigra pars reticulata (SNR)
and a secondary striatal projection area, such as subthalamic nucleus
(STN), in rats. The activity of CO was determined by measuring staini
ng intensity on brain sections processed for CO histochemistry. We als
o examined whether intrastriatal transplants. of embryonic striatal ti
ssue could affect the lesion-induced changes in the CO activity of tho
se brain structures. Unilateral striatal lesions were found to lead to
increases in the CO activity of the GP, EP, and SNR ipsilateral to th
e lesions. By contrast, the activity of the ipsilateral STN was decrea
sed following: striatal lesions, probably due to the increased inhibit
ory effect of the GP on the STN. Intrastriatal implantation of the lat
eral ganglionic eminence (LGN), but not the medial ganglionic eminence
(MGE), reversed the lesion-induced changes is the CO activity of the
GP and STN with concomitant attenuation of apomorphine-induced rotatio
nal asymmetry. The grafts failed to affect the activity of either the
EP or SNR. The present results indicate that striatal lesions induce c
hanges in the functional activity of basal ganglia nuclei and that the
LGE grafts placed in the damaged Striatum partly reverse the alterati
ons in the functional state of the basal ganglia circuitry. (C) 1998 A
cademic Press.