Entopeduncular lesions facilitate and thalamic lesions depress spontaneous and drug-evoked motor behavior in the hemiparkinsonian rat.
Pallidotomy is a neurosurgical procedure designed to ameliorate the akinesia and bradykinesia associated with Parkinson's disease. In the present study, the effects of pallidal-like lesions on motor behavior in the hemiparkinsonian rat were compared to the effects of lesions in the ventrolateral thalamus, a target of entopeduncular projections feeding motor-related information to motor cortex. Six aspects of spontaneous and evoked behavior induced by amphetamine and apomorphine in the hemiparkinsonian rat with either bilateral electrolytic entopeduncular lesions or bilateral electrolytic ventrolateral thalamic lesions were measured for 60 min. Saline or amphetamine, 5 mg/kg, or apomorphine, 0.3 mg/kg, were administered IP 5 min before the tests. The results show that on all measures except time spent resting the hemiparkinsonian rats with the entopeduncular lesions were more active than the hemiparkinsonian rats with the thalamic lesions. The asymmetrical rotation responses to dopamine receptor stimulation evoked by amphetamine and apomorphine were influenced by the general effect on gross motor behavior, as shown by the response being very large in the entopeduncular group and very small in the thalamic group. These results are consistent with current thinking about the functional organization of the basal ganglia according to which damage of the entopeduncular nucleus reduces its inhibitory control of the thalamic motor regions, thereby promoting thalamic facilitation of motor cortex, and damage to the thalamic motor regions has the opposite effect. These effects of the lesions translate, respectively, into hyperactivity and hypoactivity without blocking the asymmetrical rotation response of the hemiparkinsonian rat.
Olds
M E
ME
Division of Biology, 156-29, California Institute of Technology, Pasadena, CA 91125, USA.
Jacques
D B
DB
Kopyov
O
O
D000661:Amphetamine / Q000009:adverse effects; D000818:Animals; D001058:Apomorphine / Q000009:adverse effects; D003714:Denervation; D004195:Disease Models, Animal; D018491:Dopamine Agonists; D004409:Dyskinesia, Drug-Induced / Q000503:physiopathology / Q000601:surgery*; D020392:Entopeduncular Nucleus / Q000503:physiopathology / Q000601:surgery*; D008297:Male; D009044:Motor Cortex / Q000503:physiopathology; D009433:Neural Inhibition / Q000502:physiology; D009434:Neural Pathways / Q000503:physiopathology; D019635:Neurosurgical Procedures; D016627:Oxidopamine; D020734:Parkinsonian Disorders / Q000503:physiopathology / Q000601:surgery*; D051381:Rats; D013788:Thalamus / Q000503:physiopathology / Q000601:surgery*; D020651:Ventral Thalamic Nuclei / Q000503:physiopathology / Q000601:surgery
D018491:Dopamine Agonists; D016627:Oxidopamine; D000661:Amphetamine; D001058:Apomorphine