Asymmetry of sympathetic activity in a rat model of Parkinson's disease induced by 6-hydroxydopamine: haemodynamic, electrocardiographic and biochemical changes.
We studied the effects of experimental hemiparkinsonism upon sympathetic function in rat. The rats were divided into three groups: a group given intact control, one given lesioning with 6-hydroxydopamine (6-OHDA), and one given sham operation. One day after apomorphine testing following lesioning of the substantia nigra (SN) with 6-OHDA, heart rate (HR), mean arterial blood pressure (MAP), and electrocardiogram (ECG) were monitored. Plasma norepinephrine (NE), epinephrine (E), and dopamine (DA) levels were measured. Thereafter, immunohistochemical examination was performed to detect the extent of 6-OHDA lesions, using the avidinbiotinylated peroxidase complex (ABC) method. There was no difference in the total number of tyrosine hydroxylase (TH)-positive cells and rotation responses between the right- and left-sided 6-OHDA-treated groups. On the other hand, injury of rats with unilateral 6-OHDA resulted in haemodynamic, electrocardiographic, and biochemical changes. A significant difference was found between the right-sided 6-OHDA-treated rats and the left-sided treated ones. The MAP increased in the group given left 6-OHDA treatment and to lesser extent in the sham-operated group. In contrast, MAP did not increase in the group given right 6-OHDA treatment and was significantly lower than values in both the intact control rats and the sham-treated rats. Also, only the group given right 6-OHDA injury showed a fall in the value of HR. The plasma NE level was significantly decreased in the group given right 6-OHDA treatment compared with all other groups (P < 0.005). Our results indicate that right-sided lesioning of the nigrostriatal DA pathway in the central nervous system (CNS) has greater sympathetic consequences than left-sided ones. These results also suggest that there is a differential effect of right-sided SN lesions on sympathetic cardiac innervation. The mechanism behind the confronting impairment of autonomic nervous system (ANS) could in this experiment be attributable to an asymmetric representation of sympathetic function in the brain. However, further studies will be needed before final conclusions can be made.
Turgut
M
M
Department of Neurosurgery, Haukeland Hospital, Bergen, Norway. turgutm@adu.edu.tr
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D001522:Behavior, Animal / Q000187:drug effects; D002395:Catecholamines / Q000097:blood; D004195:Disease Models, Animal; D004562:Electrocardiography; D007839:Functional Laterality; D006439:Hemodynamics; D007150:Immunohistochemistry; D008297:Male; D016627:Oxidopamine; D010300:Parkinson Disease / Q000378:metabolism / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D013378:Substantia Nigra / Q000201:enzymology / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000201:enzymology / Q000378:metabolism / Q000503:physiopathology*; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
D002395:Catecholamines; D016627:Oxidopamine; D014446:Tyrosine 3-Monooxygenase; D001058:Apomorphine