Seizures strongly activate the endocannabinoid system. For antiseizure effects, the upregulation of CB1 activity is vital. To study seizures in mice, they are injected with kainic acid, which causes seizures, resulting in a rise of hippocampal anandamide levels. When cultures of neurons are taken from the hippo, it is seen that CB1 agonists result in discharges that are prolonged and similar to seizures, whereas these discharges are removed by CB1 antagonists. Only those discharges are removed by CB1 antagonists which lack the protective pyramidal-cell CB1 expression.
Wild-type mice have less severe and short seizures in reaction to kainic acid as compared to conditional lab mice, who undergo prolonged seizures. Both of these are in contrast to viral-vector-mediated over in hippocampal pyramidal. Seizures induced experimentally are improved when endocannabinoids’ metabolic degradation is reduced.
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This scientific study could be accelerated by relaxing the regulation of cannabis-derived drugs. Especially, the relaxation should be made for drugs which can’t potentially be abused because they contain a large quantity of non-psychoactive cannabinoids. A few states have legalised medical cannabis, but neither this nor the strength of anecdotes is enough. There is a need for double-blind, randomised and placebo-controlled, consistent clinical trials because only through these can we collect reliable insight on the safety and effectiveness of the product.