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Consumption of a selective CB-1 agonist such as ACPA protects neurons against MDMA toxicity in the amygdala
In ‘NMDA receptor adjusted co-administration of ecstasy and cannabinoid receptor-1 agonist in the amygdala via stimulation of BDNF/Trk-B/CREB pathway in adult male rats’, Ashabi and colleagues (2017) noted that NMDA blockade reduced neuronal firing rate and Tyrosine-kinase B/Brain-derived neurotrophic factor/cAMP response element binding protein level in MDMA and CB1 receptor agonist co-injected rats.
Glutamatergic system regulates the protective role of MDMA and ACPA combination via TrK-B receptors.
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CB1 receptor activation or MDMA induction reduced neuronal firing rate. Simultaneous injection of these two drugs enhanced neuronal cell survival, and these events were reversed via NMDA receptors antagonist.
Probably, the protective role of glutamatergic receptors might be through activation of BDNF/Trk-B pathways.
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