Cannabinoids in the Treatment of Dyskinetic Behaviour | cannabisMD

Cannabinoids in the Treatment of Dyskinetic Behaviour

Cannabinoids in the Treatment of Dyskinetic Behaviour; National Institute of Health

National Institute of Health

The cannabinoid agonist WIN55212-2 decreases L-DOPA induced PKA activation and dyskinetic behavior in 6-OHDA treated rats

Cannabinoids are found in the marijuana plant (cannabis sativa) and are said to be an effective anti inflammatory in treating symptoms arising from disorders such as multiple sclerosis, diabetic neuropathy, peripheral neuropathy and nausea and vomiting. A cannabinoid is one of a great collection of complex chemical compounds that naturally occur in the body and operates on major cannabinoid receptors in cells that mediates neurotransmitter release in the brain. Endogenous cannabinoids for these receptors include the endocannabinoid system, that are produced in the body by animals, the plant cannabinoids in cannabis and some other plants, and synthetic cannabinoids. The main cannabinoid is the phytocannabinoid tetrahydrocannabinol (THC), the primary psychoactive chemical in cannabis. Cannabidiol (CBD) is another main constituent of the plant and produces a non psychotic effect. This paper will review a synthetic cannabinoid and it’s ability in treating dyskinetic behaviour in rats.

Main Points

  • Cannabinoids have a role in treating motor disturbances
  • Cannabinoids have a therapeutic potential in treating motor disturbances

Cannabinoids have a role in treating motor disturbances

Chronic Levodopa (L-DOPA), the bar set for Parkinson’s disease (PD) treatment, curates crippling motor complexities (dyskinesias) that are related to modulations in the functioning of striatal protein kinase A (PKA) and cAMP-regulated phosphoprotein of 32 KDa (DARPP-32). In this research, it was illustrated that systemic dosing of the cannabinoid agonist WIN55212-2 alleviated L-DOPA-induced not your average unstable motility in the 6-OHDA rat model of PD and reversed L-DOPA-induced PKA hyperactivity by way of the CB1-controlled action. This impact was teamed with a higher rate of phosphorylation of DARPP-32 at threonine 34, which was slightly deprived by CB1 antagonism. Striatal PKA functioning was successfully correlated with the seriousness of L-DOPA-induced axial and limb dyskinesias, indicating a job for the cAMP/PKA transmissioning pathway in the conveyance of these motor disorders.

Cannabinoids have a therapeutic potential in treating motor disturbances

Overall, this research further spurs on the idea that the cAMP/PKA transmissioning pathway plays a massive role in the expression of L-DOPA-induced involuntary movements in 6-OHDA dosed rats and indicates that systemic dosing of cannabinoid agonists may give analgesic relief by reversing the abnormal L-DOPA-evoked downstream transmissioning that may be due to long-term maladaptive modulations in striatal plasticity.

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