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Immunocytochemical characterization of catecholaminergic neurons in the rat striatum following dopamine-depleting lesions

It is possible either permanently or transiently to deplete the rat striatum of dopamine. Following such depletions, striatal neurons immunoreactive for tyrosine hydroxylase (TH), aromatic l‐amino acid decarboxylase (AADC) or dopamine appear. The presence of dopamine‐producing neurons in the striatu...

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Published in:The European journal of neuroscience 1999-10, Vol.11 (10), p.3585-3596
Main Authors: Meredith, G. E., Farrell, T., Kellaghan, P., Tan, Yun, Zahm, D. S., Totterdell, S.
Format: Article
Language:English
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Summary:It is possible either permanently or transiently to deplete the rat striatum of dopamine. Following such depletions, striatal neurons immunoreactive for tyrosine hydroxylase (TH), aromatic l‐amino acid decarboxylase (AADC) or dopamine appear. The presence of dopamine‐producing neurons in the striatum has relevance for the treatment of Parkinson's disease, but whether these catecholaminergic phenotypes all produce dopamine is unclear. In the present study we establish that after unilateral 6‐hydroxydopamine lesions or methamphetamine administration, striatal TH‐immunoreactive neurons differ in size, morphology and location from those that are immunopositive for AADC or dopamine. The TH‐positive cells which were localized either to ventral parts of the striatum or to the central and dorsal areas of the caudate‐putamen generally have the morphological features of projection neurons, whereas those containing AADC or dopamine were confined to subcallosal positions in the dorsal medial quadrant of the caudate‐putamen and resemble small, local‐circuit neurons. The fact that AADC‐immunoreactive neurons overlap in size, morphology and location with the cells that produce dopamine suggests strongly that this population is dopaminergic. However, the simultaneous appearance of neurons that contain the TH enzyme but clearly do not make dopamine raises questions about the functional role of these cells and the cellular mechanisms responsible for their induction following striatal dopamine loss.
ISSN:0953-816X
1460-9568
DOI:10.1046/j.1460-9568.1999.00774.x