Your browser doesn't support javascript.
loading
[Spinophilin gene expression in 6-OHDA-lesioned rat model of parkinson's disease and L-DOPA-induced dyskinesia]
Arab Journal of Pharmaceutical Sciences. 2010; 4 (3): 136-144
in En, Ar | IMEMR | ID: emr-117877
Responsible library: EMRO
ABSTRACT
The hypothesis that alterations of proteins that mediate dopaminergic signal transduction might be involved in the altered dopaminergic receptors in Parkinson's disease and L-DOPA-induced dyskinesia was explored. We measured transcript expression of spinophilin, a protein enriched in.dendritic spines that modulates excitatory neurotransmission and involved in dopamine [DA] signaling in the striatum and cerebral cortex of 6- hydroxydopamine [6-OHDA-lesioned rats model of Parkinson's disease and following chronic treatment with L-DOPA which induces dyskinesia [L-DOPA-induced dyskinesia LID]. The transcript encoding spinophilin, was decreased by 27% and 18% respectively in, lesioned and unlesioned sides of the rostral striatum. Acute and chronic treatment with L- DOPA produced an increase in transcript levels of spinophilin in the rostral and caudal striatum, and somatosensory cortex but not in the motor cortex. These alterations in spinophilin and mRNA levels in 6-OHDA-Iesioned rat model of Parkinson's disease and L-DOPA-induced dyskinesia provide further evidence for the role of spinophilin in the neural mechanisms underlying altered dopaminergic receptors in PD and LID
Subject(s)
Search on Google
Index: IMEMR Main subject: Rats / Levodopa / Gene Expression / Receptors, Dopamine / Oxidopamine / Models, Animal / Dyskinesia, Drug-Induced / Microfilament Proteins / Nerve Tissue Proteins / Antiparkinson Agents Limits: Animals Language: Ar / En Journal: Arab J. Pharm. Sci. Year: 2010
Search on Google
Index: IMEMR Main subject: Rats / Levodopa / Gene Expression / Receptors, Dopamine / Oxidopamine / Models, Animal / Dyskinesia, Drug-Induced / Microfilament Proteins / Nerve Tissue Proteins / Antiparkinson Agents Limits: Animals Language: Ar / En Journal: Arab J. Pharm. Sci. Year: 2010