ArticleNoro psikiyatri arsivi2018
Striatal Neurotransmitter Release-related Presynaptic Proteins in L-dopa Induced Dyskinesia in a Model of Parkinsonism.
Article in Noro psikiyatri arsivi, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 0 citations in OpenAlex.
- Remodeling of Perineuronal Nets in the Striato-Cortical Axis in L-DOPA-Induced Dyskinesia Rat Model.International journal of molecular sciences · 2025Article
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
introductionIn Parkinson's disease, L-dopa-induced dyskinesia (LID) and motor fluctuations incapacitate patients as much as the disease itself. Many studies demonstrated that postsynaptic alterations and striatal synaptic plasticity changes play a role in LID development. Here, we aimed to study the role of striatal presynaptic proteins in LID pathogenesis.
methodsFor this purpose, 6-hydroxydopamine model of parkinsonism was used. To induce LID, these rats were treated with intraperitoneal injections of L-dopa 25 mg/kg with benserazide 6.25 mg/kg b.i.d for 21 days. Rats with parkinsonism treated with saline and control rats treated with saline or L-dopa/ benserazide were also included. Behaviors of rats were videotaped and scored according to dyskinesia scale. Striatal tissue was analysed with immunofluorescence staining and immunoblotting to confirm loss of tyrosine hydroxylase (TH) expression due to dopaminergic denervation and to explore the alterations in the expression of presynaptic proteins, secretogranin 2 (SG2), synaptophysin (Syp) and synaptotagmin 7 (Syt7).
resultLID developed only in rats with parkinsonism treated with chronic L-dopa. Immunofluorescence and immunoblotting studies for TH confirmed depletion of dopaminergic neurons, which was also strongly and negatively correlated with severity of LID. Striatal SG2 and Syp levels were found increased in parkinsonian rats. Chronic L-dopa treatment further increased SG2 levels in denervated striatum. Striatal SG 2 level showed a significant moderate, positive correlation with LID severity. Immunofluorescence studies also demonstrated increased expression of these presynaptic proteins in the denervated striatum.
conclusionAs, severity of LID was clearly correlated with striatal SG2 expression; there is supposedly a functional relationship between striatal SG2 and LID. Further studies are needed to find out molecular mechanisms linking increased SG2 expression and LID.
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