Objective: Cannabinoids have been demonstrated to be effective in preclinical studies involving oxidative stress, neuroinflammation, and motor complications associated with Parkinson’s disease (PD).The CB1 cannabinoid receptors are abundantly expressed in the basal ganglia, the circuitry that is mostly affected in PD.

Background: In this study we investigated effect of Arachidonyl-2′-chloroethylamide (ACEA) as a CB1 receptor agonist in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced PD model in mices to assess the neuroprotective role of ACEA in slowing down of PD progression and improvement of motor function.

Methods: Forty-five mices were divided to three groups. One group were injected MPTP(systemically) as a control group. Second group were injected MPTP and then ACEA, 7 days after injection of MPTP to assess preservation of dopamine function in brain. In the third group after 2 days of pretreatment with ACEA (intraperitoneal), MPTP were injected to assay neuroprotection effect of ACEA.

Results: Behavioral analysis showed significant improvement in ACEA pretreatment group. Also neurochemical analysis that were used to assess dopamine metabolites and small-scale immunohistochemistry studies after brain resection showed significant rise in dopamine metabolites, CB1 receptors upregulation and survival of dopaminergic neurons in compared with controls.

Conclusions: Our data indicates that ACEA as a CB1 receptor agonist protects against MPTP-induced nigrostriatal degeneration by inhibiting microglial cells activation that suggests ACEA as a new therapeutic target to slow down the degenerative process occurring and to improve motor function in PD.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/effects-of-arachidonyl-2-chloroethylamide-acea-a-selective-cb1-receptor-agonist-in-mptp-mouse-model-of-parkinsons-disease/