engleski

Phenotypic characterization of tyrosine hydroxilase immunoreactive striatal neurons in the 6-OHDA lesioned mice.

Neurons immunoreactive for tyrosine hydroxilase (TH-ir) could be observed in a rodent striatum after dopamine depletion. Immunocytochemistry studies demonstrated that morphologies of these cells correspond to striatal neurons, however the lack of lipofuscin that is normally present in the striatal neurons, suggest otherwise. In the present study, we have examined if these cells are newborn striatal neurons, their time-course of appearance and their phenotypic characteristics in the striatum of mice lesioned with 6-OHDA. TH-ir neuronal density was measured 0.5, 1, 2 and 7 weeks after lesion using a Neurolucida system. The possible birth of new TH-ir neurons following the lesion was investigated by BrdU incorporation. Phenotype characterization was performed by fluorescent double immunolabeling combining a TH antiserum and markers of different striatal neuronal populations or dopaminergic markers. TH-ir neurons could be observed from 3 days after lesion, but their density and the intensity of TH staining progressively decreased, being one order of magnitude less at 7 weeks after the lesion. We did not detect any TH-positive neuron expressing BrdU in the lesioned striatum. TH-positive neurons expressed mainly dynorphin (54 %) and enkephalin (45%), indicating that these neurons are striatal projection neurons. In respect to striatal interneurons, we found that about 1 % of these cells expressed calretinin, but did not express choline acetyl transferase, parvalbumine or somastostatin. Interestingly, these neurons did not express DAT and about 1% of TH-ir neurons expressed aromatic-L-amino acid decarboxylase. In summary our results indicate that the appearance of TH-ir neurons after 6-OHDA lesion in the mice stratum is caused by a transient expression of TH in both populations of striatal projection neurons without expression of other dopaminergic markers.

aromatic-L-amino acid decarboxylase; basal ganglia; dopamine transporter; dynorphin; enkephalin; L-3; 4-dihydroxyphenylalanine; neurogenesis; Parkinson’s disease

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