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

Citation
Ge. Meredith et al., Immunocytochemical characterization of catecholaminergic neurons in the rat striatum following dopamine-depleting lesions, EUR J NEURO, 11(10), 1999, pp. 3585-3596
Citations number
69
Categorie Soggetti
Neurosciences & Behavoir
Journal title
EUROPEAN JOURNAL OF NEUROSCIENCE
ISSN journal
0953816X → ACNP
Volume
11
Issue
10
Year of publication
1999
Pages
3585 - 3596
Database
ISI
SICI code
0953-816X(199910)11:10<3585:ICOCNI>2.0.ZU;2-C
Abstract
It is possible either permanently or transiently to deplete the rat striatu m of dopamine. Following such depletions, striatal neurons immunoreactive f or tyrosine hydroxylase (TH), aromatic L-amino acid decarboxylase (AADC) or dopamine appear. The presence of dopamine-producing neurons in the striatu m has relevance for the treatment of Parkinson's disease, but whether these catecholaminergic phenotypes all produce dopamine is unclear. In the prese nt study we establish that after unilateral 6-hydroxydopamine lesions or me thamphetamine administration, striatal TH-immunoreactive neurons differ in size, morphology and location from those that are immunopositive for AADC o r dopamine. The TH-positive cells which were localized either to ventral pa rts of the striatum or to the central and dorsal areas of the caudate-putam en generally have the morphological features of projection neurons, whereas those containing AADC or dopamine were confined to subcallosal positions i n the dorsal medial quadrant of the caudate-putamen and resemble small, loc al-circuit neurons. The fact that AADC-immunoreactive neurons overlap in si ze, morphology and location with the cells that produce dopamine suggests s trongly that this population is dopaminergic. However, the simultaneous app earance of neurons that contain the TH enzyme but clearly do not make dopam ine raises questions about the functional role of these cells and the cellu lar mechanisms responsible for their induction following striatal dopamine loss.