Changes in the mitochondrial enzyme activity in striatal projection areas after unilateral excitotoxic striatal lesions: partial restoration by embryonic striatal transplants.
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 activity in primary striatal targets, including the globus pallidus (GP), entopeduncular 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 staining intensity on brain sections processed for CO histochemistry. We also examined whether intrastriatal transplants of embryonic striatal tissue could affect the lesion-induced changes in the CO activity of those brain structures. Unilateral striatal lesions were found to lead to increases in the CO activity of the GP, EP, and SNR ipsilateral to the lesions. By contrast, the activity of the ipsilateral STN was decreased following striatal lesions, probably due to the increased inhibitory effect of the GP on the STN. Intrastriatal implantation of the lateral ganglionic eminence (LGN), but not the medial ganglionic eminence (MGE), reversed the lesion-induced changes in the CO activity of the GP and STN with concomitant attenuation of apomorphine-induced rotational asymmetry. The grafts failed to affect the activity of either the EP or SNR. The present results indicate that striatal lesions induce changes in the functional activity of basal ganglia nuclei and that the LGE grafts placed in the damaged striatum partly reverse the alterations in the functional state of the basal ganglia circuitry.
Department of Neurological Surgery, Wakayama Medical College, Wakayama, 7-27, Japan.
N
N
Nakao
K
K
Nakai
T
T
Itakura
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001921:Brain / Q000201:enzymology*; D016380:Brain Tissue Transplantation / Q000502:physiology*; D003342:Corpus Striatum / Q000502:physiology* / Q000637:transplantation*; D051937:Dopamine and cAMP-Regulated Phosphoprotein 32; D003576:Electron Transport Complex IV / Q000378:metabolism*; D016332:Fetal Tissue Transplantation / Q000502:physiology; D007839:Functional Laterality; D005917:Globus Pallidus / Q000201:enzymology; D008297:Male; D008928:Mitochondria / Q000201:enzymology*; D008959:Models, Neurological; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology*; D009419:Nerve Tissue Proteins / Q000032:analysis; D009928:Organ Specificity; D010750:Phosphoproteins / Q000032:analysis; D017378:Quinolinic Acid / Q000633:toxicity; D051381:Rats; D017207:Rats, Sprague-Dawley; D013378:Substantia Nigra / Q000201:enzymology; D013787:Thalamic Nuclei / Q000201:enzymology
D051937:Dopamine and cAMP-Regulated Phosphoprotein 32; D009419:Nerve Tissue Proteins; D010750:Phosphoproteins; D003576:Electron Transport Complex IV; D017378:Quinolinic Acid; D001058:Apomorphine