Providing further evidence that marijuana is indeed a miracle plant, a recently published study in the May issue ofthe Journal PLOS ONE and online by the National Institute of Health has uncovered an interesting cannabinoid secret: marijuana’s main psychoactive cannabinoid – THC, a.k.a. tetrahydrocannabinol – can potentially minimize, if not prevent, the ugly and insidious brain damage brought on by methamphetamine use.
cannabinoids, THC and methamphetamines
According to the study’s methodology, “Preclinical studies have shown that natural (Δ9-tetrahydrocannabinol, Δ9-THC) and synthetic cannabinoid CB1 and CB2 receptor agonists exert neuroprotective effects on different models of cerebral damage. In this recent study, researchers investigated the neuroprotective effect of Δ9-THC on METH-induced neurotoxicity by examining its ability to reduce astrocyte activation and nNOS over-expression in selected brain areas.
Testing their hypothesis, the researchers subjected rats exposed to methamphetamine’s neurotoxic regime (approximately two hours apart) and were pre- or post-treated with marijuana’s THCcannabinoid. The results were nothing short of astounding.
“Compared to corresponding controls (i) METH-induced nNOS overexpression in the caudate-putamen (CPu) was significantly attenuated by pre- and post-treatment with both doses of Δ9-THC (-19% and -28% for 1 mg/kg pre- and post-treated animals; -25% and -21% for 3 mg/kg pre- and post-treated animals); (ii) METH-induced GFAP-immunoreactivity (IR) was significantly reduced in the CPu by post-treatment with 1 mg/kg Δ9-THC1 (-50%) and by pre-treatment with 3 mg/kg Δ9-THC (-53%); (iii) METH-induced GFAP-IR was significantly decreased in the prefrontal cortex (PFC) by pre- and post-treatment with both doses of Δ9-THC (-34% and -47% for 1 mg/kg pre- and post-treated animals; -37% and -29% for 3 mg/kg pre- and post-treated animals).
Leaving researchers with only one conclusion: “Our results indicate that Δ9-THC reduces METH-induced brain damage via inhibition of nNOS expression and astrocyte activation through CB1-dependent and independent mechanisms, respectively.”
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