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Mechanisms of Antiparkinsonian Anticholinergic Therapy Revisited.
Neuroscience
July 2021
Universidad de Buenos Aires, CONICET, Instituto de Fisiología y Biofísica (IFIBIO) Bernardo Houssay, Grupo de Neurociencia de Sistemas, 2155 Paraguay Street, Buenos Aires 1121, Argentina. Electronic address:
Before the advent of L-DOPA, the gold standard symptomatic therapy for Parkinson's disease (PD), anticholinergic drugs (muscarinic receptor antagonists) were the preferred antiparkinsonian therapy, but their unwanted side effects associated with impaired extrastriatal cholinergic function limited their clinical utility. Since most patients treated with L-DOPA also develop unwanted side effects such as L-DOPA-induced dyskinesia (LID), better therapies are needed. Recent studies in animal models demonstrate that optogenetic and chemogenetic manipulation of striatal cholinergic interneurons (SCIN), the main source of striatal acetylcholine, modulate parkinsonism and LID, suggesting that restoring SCIN function might serve as a therapeutic option that avoids extrastriatal anticholinergics' side effects.
View Article and Find Full Text PDFLevodopa Causes Striatal Cholinergic Interneuron Burst-Pause Activity in Parkinsonian Mice.
Mov Disord
July 2021
Universidad de Buenos Aires, CONICET, Instituto de Fisiología y Biofísica (IFIBIO) Bernardo Houssay, Grupo de Neurociencia de Sistemas, 2155 Paraguay Street, Buenos Aires, 1121, Argentina.
Background: Enhanced striatal cholinergic interneuron activity contributes to the striatal hypercholinergic state in Parkinson's disease (PD) and to levodopa-induced dyskinesia. In severe PD, dyskinesia and motor fluctuations become seriously debilitating, and the therapeutic strategies become scarce. Given that the systemic administration of anticholinergics can exacerbate extrastriatal-related symptoms, targeting cholinergic interneurons is a promising therapeutic alternative.
View Article and Find Full Text PDFStriatal and nigral muscarinic type 1 and type 4 receptors modulate levodopa-induced dyskinesia and striato-nigral pathway activation in 6-hydroxydopamine hemilesioned rats.
Neurobiol Dis
October 2020
Department of Biomedical and Specialty Surgical Sciences, Section of Pharmacology, University of Ferrara, 44122 Ferrara, Italy. Electronic address:
Acetylcholine muscarinic receptors (mAChRs) contribute to both the facilitation and inhibition of levodopa-induced dyskinesia operated by striatal cholinergic interneurons, although the receptor subtypes involved remain elusive. Cholinergic afferents from the midbrain also innervate the substantia nigra reticulata, although the role of nigral mAChRs in levodopa-induced dyskinesia is unknown. Here, we investigate whether striatal and nigral M1 and/or M4 mAChRs modulate dyskinesia and the underlying striato-nigral GABAergic pathway activation in 6-hydroxydopamine hemilesioned rats.
View Article and Find Full Text PDFGalantamine in rheumatoid arthritis: A cross talk of parasympathetic and sympathetic system regulates synovium-derived microRNAs and related pathogenic pathways.
Eur J Pharmacol
September 2020
Department of Biochemistry, Medical Research Institute, Alexandria University, Alexandria, Egypt.
The acetylcholinesterase inhibitor, galantamine, has shown therapeutic effect in rat model of rheumatoid arthritis. Hence, the current study aims at determining the mode of action of galantamine by examining different synovium-derived microRNAs (miRs) and their related pathogenic pathways. The study also focuses on how parasympathetic and sympathetic pathways in the synovial tissue could affect the mode of action and anti-arthritic effect of galantamine.
View Article and Find Full Text PDFAcetylcholinesterase inhibitory activity and neuroprotection in vitro, molecular docking, and improved learning and memory functions of demethylcurcumin in scopolamine-induced amnesia ICR mice.
Food Funct
March 2020
Department of General Medicine, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
In this study, demethylcurcumin (DC), a minor constituent in curcuminoids, showed better anti-acetylcholinesterase (anti-AChE) activities, anti-amyloid β peptide aggregation, neuroprotective activities in 6-hydroxydopamine-treated SH-SY5Y cell models, and anti-nitric oxide production in lipopolysaccharide-treated RAW 264.7 macrophages than those of curcumin. Based on molecular docking analyses with AChE, the meta-hydroxyl group in DC, nonexistent in curcumin, showed the formation of hydrogen bonds with Ser293 and Tyr341 in the binding sites of AChE.
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