Subthalamic nucleus lesion in rats prevents dopaminergic nigral neuron degeneration after striatal 6-OHDA injection: Behavioural and immunohistochemical studies
European Journal of Neuroscience. 1996-07-01; 8(7): 1408-1414
DOI: 10.1111/j.1460-9568.1996.tb01603.x
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1. Eur J Neurosci. 1996 Jul;8(7):1408-14. doi:
10.1111/j.1460-9568.1996.tb01603.x.
Subthalamic nucleus lesion in rats prevents dopaminergic nigral neuron
degeneration after striatal 6-OHDA injection: behavioural and
immunohistochemical studies.
Piallat B(1), Benazzouz A, Benabid AL.
Author information:
(1)Laboratoire de Neurobiologie Préclinique, INSERM U.318, CHU, Pavillon B, BP
217, 38043 Grenoble Cedex 09, France.
Several studies have shown that antagonists of N-methyl-D-aspartate receptors
provide protection of the dopaminergic nigrostriatal pathway in animal models of
Parkinson’s disease. Since the substantia nigra compacta receives a moderate
glutamatergic innervation from the subthalamic nucleus, we tried to determine
whether subthalamic nucleus lesion could prevent the toxicity of the selective
dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA). Experiments were carried out
on four groups of rats. Group 1 (n = 10) received a unilateral injection of
6-hydroxydopamine in the striatum and group 2 (n = 10) received kainic acid in
the subthalamic nucleus. Group 3 (n = 10) received an injection of kainic acid
in the subthalamic nucleus and 1 week later an injection of 6-OHDA in the
striatum. Group 4 (n = 5) received the same treatment but kainic acid was
replaced by saline. Apomorphine induced an ipsilateral rotation in rats of
groups 2 and 3 and a contralateral rotation in rats of groups 1 and 4. The
number of tyrosine hydroxylase-immunoreactive cells in the pars compacta of the
substantia nigra was not significantly decreased on the side ipsilateral to
6-OHDA striatal injection in rats of groups 1 and 4. These results show that
subthalamic nucleus lesion provides neuroprotection of the dopaminergic
nigrostriatal pathway against 6-OHDA toxicity and opens a new way for slowing or
stopping the progression of Parkinson’s disease.
DOI: 10.1111/j.1460-9568.1996.tb01603.x
PMID: 8758948 [Indexed for MEDLINE]