Cannabidiol attenuates methamphetamine-induced psychosis via anti-oxidative stress: σ1R-mediated mitochondrial
Liu Liu1, Chan Wang1, Yunqing Tian1
1NHC Key Laboratory of Drug Addiction Medicine, School of Forensic Medicine, Kunming Medical University, Kunming, Yunnan, PR China.
Summary
Cannabidiol (CBD) effectively treats methamphetamine-induced psychosis (MIP) symptoms in mice by reducing oxidative stress and calcium overload via the Sigma-1 receptor (σ1R). This research highlights CBD as a potential therapeutic agent for MIP.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Methamphetamine-induced psychosis (MIP) affects a significant portion of chronic methamphetamine users, with unclear causes and treatments.
- Cannabidiol (CBD), a neuroprotective compound, shows promise for neuropsychiatric disorders due to its antioxidant properties.
Purpose of the Study:
- To investigate the therapeutic mechanisms of CBD against MIP.
- To focus on the role of Sigma-1 receptor (σ1R)-mediated mitochondrial dysfunction in CBD's effects.
Main Methods:
- Utilized in vitro and in vivo models of methamphetamine exposure.
- Assessed MIP behaviors and performed molecular analyses of oxidative stress and mitochondrial function in mouse hippocampus and HT22 cells.
- Employed genetic strategies to modulate σ1R, and used molecular dynamics and SPR to study CBD-σ1R interactions.
Main Results:
- CBD (40 mg/kg) reduced anxiety-like behaviors and cognitive deficits in mice exposed to methamphetamine.
- CBD mitigated neuronal damage, mitochondrial superoxide production, and calcium dysregulation.
- Neuroprotection was linked to σ1R function, confirmed by genetic modulation and molecular binding studies.
Conclusions:
- CBD alleviates MIP-related behavioral and cognitive impairments in mice.
- CBD's therapeutic effects stem from attenuating σ1R-mediated mitochondrial oxidative stress and calcium overload.
- The findings support CBD as a potential treatment for methamphetamine-induced psychosis.
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