Entopeduncular lesions facilitate and thalamic lesions depress spontaneousand drug-evoked motor behavior in the hemiparkinsonian rat

Citation
Me. Olds et al., Entopeduncular lesions facilitate and thalamic lesions depress spontaneousand drug-evoked motor behavior in the hemiparkinsonian rat, SYNAPSE, 40(3), 2001, pp. 215-224
Citations number
28
Categorie Soggetti
Neurosciences & Behavoir
Journal title
SYNAPSE
ISSN journal
08874476 → ACNP
Volume
40
Issue
3
Year of publication
2001
Pages
215 - 224
Database
ISI
SICI code
0887-4476(20010601)40:3<215:ELFATL>2.0.ZU;2-0
Abstract
Pallidotomy is a neurosurgical procedure designed to ameliorate the akinesi a and bradykinesia associated with Parkinson's disease. In the present stud y, the effects of pallidal-like lesions on motor behavior in the hemiparkin sonian rat were compared to the effects of lesions in the ventrolateral tha lamus, a target of entopeduncular projections feeding motor-related informa tion to motor cortex. Six aspects of spontaneous and evoked behavior induce d by amphetamine and apomorphine in the hemiparkinsonian rat with either bi lateral electrolytic entopeduncular lesions or bilateral electrolytic ventr olateral 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 t ests. The results show that on all measures except time spent resting the h emiparkinsonian rats with the entopeduncular lesions were more active than the hemiparkinsonian rats with the thalamic lesions. The asymmetrical rotat ion responses to dopamine receptor stimulation evoked by amphetamine and ap omorphine were influenced by the general effect on gross motor behavior, as shown by the response being very large in the entopeduncular group and ver y small in the thalamic group. These results are consistent with current th inking about the functional organization of the basal ganglia according to which damage of the entopeduncular nucleus reduces its inhibitory control o f the thalamic motor regions, thereby promoting thalamic facilitation of mo tor cortex, and damage to the thalamic motor regions has the opposite effec t. These effects of the lesions translate, respectively, into hyperactivity and hypoactivity without blocking the asymmetrical rotation response of th e hemiparkinsonian rat. Synapse 40:215-224, 2001. (C) 2001 Wiley-Liss. Inc.