Intrastriatal angiotensin II induces turning behaviour in 6-hydroxydopamine lesioned rats

• Published in: Brain research Vol. 691; no. 1; pp. 213 - 216
• Main Authors: Jenkins, T.A., Chai, S.Y., Howells, D.W., Mendelsohn, F.A.O.
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 11-09-1995; Amsterdam Elsevier; New York, NY
• Subjects: Anatomical correlates of behavior; Angiotensin II; Angiotensin II - antagonists & inhibitors; Angiotensin II - pharmacology; Animals; Behavioral psychophysiology; Biological and medical sciences; Biphenyl Compounds - pharmacology; Corpus Striatum - drug effects; Dopamine; Dopamine - physiology; Functional Laterality - physiology; Fundamental and applied biological sciences. Psychology; Haloperidol; Haloperidol - pharmacology; Imidazoles - pharmacology; Losartan; Male; Motor Activity - drug effects; Oxidopamine; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Rats; Rats, Sprague-Dawley; Rotation; Striatum; Substantia nigra; Substantia Nigra - drug effects; Tetrazoles - pharmacology; Striatum; Dopamine; Losartan; Substantia nigra; Haloperidol; Angiotensin II; Rotation; Rat; Rodentia; Central nervous system; Basal ganglion; Corpus striatum; Oxidopamine; Vertebrata; Mammalia; Animal; Rotation behavior; Lesion; Brain (vertebrata)
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/0006-8993(95)00677-I

In rats with unilateral 6-hydroxydopamine lesions in the nigrostriatal pathway, injection of Angiotensin II (2 nmol) into the unlesioned striatum elicited dose-related tight rotations ipsilateral to the lesion. This rotation was suppressed by coadministration of the Angiotensin AT
1 receptor antagonist, losartan (2 nmol), which had no significant effect when injected alone. Preadministration of the dopamine antagonist, haloperidol (2 mg/kg i.p.) completely blocked angiotensin II-induced turning at doses of 0.3–3 nmol, and partially at 10 nmol. These results further confirm the hypothesis that Ang II is intrinsically involved in modulating dopamine release in the striatum, an effect which is mediated predominantly by AT
1 receptors.