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Time‐course of nigrostriatal damage, basal ganglia metabolic changes and behavioural alterations following intrastriatal injection of 6‐hydroxydopamine in the rat: new clues from an old model

Time‐course of nigrostriatal damage, basal ganglia metabolic changes and behavioural alterations... Despite the progressive development of innovative animal models for Parkinson's disease, the intracerebral infusion of neurotoxin 6‐hydroxydopamine (6‐OHDA) remains the most widely used means to induce an experimental lesion of the nigrostriatal pathway in the animal, due to its relatively low complexity and cost, coupled with the high reproducibility of the lesion obtained. To gain new information from such a classic model, we studied the time‐course of the nigrostriatal damage, metabolic changes in the basal ganglia nuclei (cytochrome oxidase activity) and behavioural modifications (rotational response to apomorphine) following unilateral injection of 6‐OHDA into the corpus striatum of rat, over a 4‐week period. Striatal infusion of 6‐OHDA caused early damage of dopaminergic terminals, followed by a slowly evolving loss of dopaminergic cell bodies in the substantia nigra pars compacta, which became apparent during the second week post‐injection and peaked at the 28th day post‐infusion; the rotational response to apomorphine was already present at the first time point considered (Day 1), and remained substantially stable throughout the 4‐week period of observation. The evolution of the nigrostriatal lesion was accompanied by complex changes in the metabolic activity of the other basal ganglia nuclei investigated (substantia nigra pars reticulata, entopeduncular nucleus, globus pallidus and subthalamic nucleus), which led, ultimately, to a generalized, metabolic hyperactivity, ipsilaterally to the lesion. However, peculiar patterns of metabolic activation, or inhibition, characterized the post‐lesional responses of each nucleus, in the early and intermediate phases, with peculiar response profiles that varied closely related to the functional position occupied within the basal ganglia circuitry. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Neuroscience Wiley

Time‐course of nigrostriatal damage, basal ganglia metabolic changes and behavioural alterations following intrastriatal injection of 6‐hydroxydopamine in the rat: new clues from an old model

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References (75)

Publisher
Wiley
Copyright
Copyright © 2007 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0953-816X
eISSN
1460-9568
DOI
10.1111/j.1460-9568.2006.05285.x
pmid
17284180
Publisher site
See Article on Publisher Site

Abstract

Despite the progressive development of innovative animal models for Parkinson's disease, the intracerebral infusion of neurotoxin 6‐hydroxydopamine (6‐OHDA) remains the most widely used means to induce an experimental lesion of the nigrostriatal pathway in the animal, due to its relatively low complexity and cost, coupled with the high reproducibility of the lesion obtained. To gain new information from such a classic model, we studied the time‐course of the nigrostriatal damage, metabolic changes in the basal ganglia nuclei (cytochrome oxidase activity) and behavioural modifications (rotational response to apomorphine) following unilateral injection of 6‐OHDA into the corpus striatum of rat, over a 4‐week period. Striatal infusion of 6‐OHDA caused early damage of dopaminergic terminals, followed by a slowly evolving loss of dopaminergic cell bodies in the substantia nigra pars compacta, which became apparent during the second week post‐injection and peaked at the 28th day post‐infusion; the rotational response to apomorphine was already present at the first time point considered (Day 1), and remained substantially stable throughout the 4‐week period of observation. The evolution of the nigrostriatal lesion was accompanied by complex changes in the metabolic activity of the other basal ganglia nuclei investigated (substantia nigra pars reticulata, entopeduncular nucleus, globus pallidus and subthalamic nucleus), which led, ultimately, to a generalized, metabolic hyperactivity, ipsilaterally to the lesion. However, peculiar patterns of metabolic activation, or inhibition, characterized the post‐lesional responses of each nucleus, in the early and intermediate phases, with peculiar response profiles that varied closely related to the functional position occupied within the basal ganglia circuitry.

Journal

European Journal of Neuroscience – Wiley

Published: Jan 1, 2007

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