Rotation evoked by nigral stimulation following lateral hypothalamic, striatal, and pallidal lesions in rats

• Published in: Experimental neurology Vol. 77; no. 2; pp. 295 - 313
• Main Authors: Saranak, Jureepan, Goldfarb, Joseph
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.08.1982
• Subjects: Animals; Corpus Striatum - physiology; Electric Stimulation; Functional Laterality; Globus Pallidus - physiology; Hydroxydopamines - pharmacology; Hypothalamus - physiology; Kinetics; Male; Motor Activity - drug effects; Oxidopamine; Rats; Rats, Inbred Strains; Rotation; Substantia Nigra - physiology; 6-OHDA; DA; NER
• ISSN: 0014-4886; 1090-2430
• DOI: 10.1016/0014-4886(82)90247-3

Contraversive rotation evoked by electrical stimulation of the rat substantia nigra (nigral-evoked rotation, NER) was not reduced by 6-hydroxydopamine (6-OHDA, 4 μg in 2 μl or 1 μg in 0.5 μl) at the ipsilateral lateral hypothalamus. These lesions produced striatal dopamine depletions equivalent to those produced by electrolytic lesions at that site which reduced NER. Electrolytic lesions at the lateral hypothalamus produced equivalent reduction in NER in rats with prior microinjection of either 6-OHDA (8 μg in 4 μl) or vehicle at that site. Thus, the decrease in NER after electrolytic lesions at the lateral hypothalamus appears to be entirely due to destruction of nondopaminergic fibers. Small electrolytic lesions at the ipsilateral caudate-putamen did not significantly change NER. Large electrolytic lesions at the caudate-putamen did not alter NER at 2 h after lesion but did reduce it at 3, 7, and 14 days postlesion. Electrolytic lesions at the ipsilateral globus pallidus significantly reduced contraversive NER at all times tested (2, 3, 7, and 14 days after lesion). Some rats with pallidal lesions responded to nigral stimulation with ipsiversive rotation. The difference in time course of the reduction in contraversive NER after caudate-putamen and pallidal lesions suggests that NER might be mediated by antidromic activitation of striatonigral neurons that send axonal collaterals to the pallidum.