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- W3208291573 abstract "Characterization of new pharmacological targets is a promising approach in research of neurorepair mechanisms. The G protein-coupled receptor 17 (GPR17) has recently been proposed as an interesting pharmacological target, e.g., in neuroregenerative processes. Using the well-established ex vivo model of organotypic slice co-cultures of the mesocortical dopaminergic system (prefrontal cortex (PFC) and substantia nigra/ventral tegmental area (SN/VTA) complex), the influence of GPR17 ligands on neurite outgrowth from SN/VTA to the PFC was investigated. The growth-promoting effects of Montelukast (MTK; GPR17- and cysteinyl-leukotriene receptor antagonist), the glial cell line-derived neurotrophic factor (GDNF) and of two potent, selective GPR17 agonists (PSB-16484 and PSB-16282) were characterized. Treatment with MTK resulted in a significant increase in mean neurite density, comparable with the effects of GDNF. The combination of MTK and GPR17 agonist PSB-16484 significantly inhibited neuronal growth. qPCR studies revealed an MTK-induced elevated mRNA-expression of genes relevant for neuronal growth. Immunofluorescence labelling showed a marked expression of GPR17 on NG2-positive glia. Western blot and RT-qPCR analysis of untreated cultures suggest a time-dependent, injury-induced stimulation of GPR17. In conclusion, MTK was identified as a stimulator of neurite fibre outgrowth, mediating its effects through GPR17, highlighting GPR17 as an interesting therapeutic target in neuronal regeneration." @default.
- W3208291573 created "2021-11-08" @default.
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- W3208291573 date "2021-10-28" @default.
- W3208291573 modified "2023-09-26" @default.
- W3208291573 title "Involvement of GPR17 in Neuronal Fibre Outgrowth" @default.
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- W3208291573 doi "https://doi.org/10.3390/ijms222111683" @default.
- W3208291573 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8584086" @default.
- W3208291573 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34769111" @default.
- W3208291573 hasPublicationYear "2021" @default.
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