Cannabidiol promotes neurogenesis in the dentate gyrus during an abstinence period in rats following chronic exposure to methamphetamine

Razavi, Yasaman; Keyhanfar, Fariborz; Haghparast, Abbas; Shabani, Ronak; Mehdizadeh, Mehdi

doi:10.1007/s11011-021-00774-9

Cited by 7 publications

(12 citation statements)

References 67 publications

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“…As CBD promotes neurogenesis in the Hip of rats under chronic METH exposure ( Razavi et al, 2021 ) and modulates the psychoactive properties of METH via DA receptors in the Hip of rats ( Hassanlou et al, 2021 ; Nouri et al, 2021 ), we repeated the above experiments in the Hip. Results showed that METH exposure induced DRD1 [ Figure 11A ; F (3, 16) = 74.578, p < 0.001], pMeCP2 [ Figure 11A ; F (3, 16) = 63.564, p < 0.001], cleaved caspase-8 [ Figure 11A ; F (3, 20) = 44.202, p < 0.001], and cleaved caspase-3 expression [ Figure 11A ; F (3, 16) = 25.338, p < 0.001] in the Hip, whereas CBD pretreatment blocked the high expression of DRD1 [ Figure 11A ; F (3, 16) = 74.578, p < 0.001], pMeCP2 [ Figure 11A ; F (3, 16) = 63.564, p < 0.001], cleaved caspase-8 [ Figure 11A ; F (3, 20) = 44.202, p < 0.001], and cleaved caspase-3 [ Figure 11A ; F (3, 16) = 25.338, p < 0.001].…”

Section: Resultsmentioning

confidence: 99%

“…CBD exhibits excellent therapeutic potential in neuropsychiatric disorders such as epilepsy, PD, AD, depression, anxiety, psychosis, and drug dependence ( Elsaid et al, 2019 ; Premoli et al, 2019 ; Vitale et al, 2021 ). Under METH exposure, CBD shows neuroprotective ( Razavi et al, 2021 ), antioxidative, and anti-inflammatory properties ( Majdi et al, 2019 ; Karimi-Haghighi et al, 2020 ). In addition, CBD can restore the adaptation to threshold doses caused by repeated METH exposure ( Khanegheini et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

“…Our results showed that CBD pretreatment prevented METH-induced caspase-8/caspase-3 cascade and apoptosis in-vitro and in-vivo . During abstinence periods, CBD has been shown to promote neurogenesis in the Hip dentate gyrus in rats under chronic METH exposure ( Razavi et al, 2021 ). In the current study, we found that CBD pretreatment markedly prevented the increase in caspase-8/caspase-3 cascade and apoptosis in the Hip of rats induced by repeated METH exposure.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, to further explore the neuroprotective effects of CBD, we investigated protein expression, intracellular Ca 2+ , and apoptosis levels in the PFC of rats. Results showed that repeated METH exposure markedly increased the expression levels of DRD1 [Figure 10A As CBD promotes neurogenesis in the Hip of rats under chronic METH exposure (Razavi et al, 2021) and modulates the psychoactive properties of METH via DA receptors in the Hip of rats (Hassanlou et al, 2021;Nouri et al, 2021)…”

Section: Cannabidiol Prevented Growth Inhibition and Stereotyped Beha...mentioning

confidence: 99%

“…Cannabidiol (CBD) is a primary non-psychoactive cannabinoid in the cannabis plant and exhibits considerable therapeutic potential in the treatment of neuropsychiatric disorders, including epilepsy, Parkinson’s disease (PD), Alzheimer’s disease (AD), depression, anxiety, psychosis, and drug dependence ( Elsaid et al, 2019 ; Premoli et al, 2019 ; Vitale et al, 2021 ). Recent research has indicated that CBD exerts neuroprotective effects on METH-induced neurotoxicity in rats ( Razavi et al, 2021 ). Furthermore, some evidence has suggested that CBD modulates several receptors in METH exposure, such as D1-like DA receptors ( Nouri et al, 2021 ; Shen et al, 2022 ), D2-like DA receptors ( Hassanlou et al, 2021 ), Sigma-1 receptors ( Yang et al, 2020 ), and Toll-like type-4 receptors (TLR4) ( Majdi et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

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Cannabidiol prevents methamphetamine-induced neurotoxicity by modulating dopamine receptor D1-mediated calcium-dependent phosphorylation of methyl-CpG-binding protein 2

et al. 2022

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In the past decade, methamphetamine (METH) abuse has sharply increased in the United States, East Asia, and Southeast Asia. METH abuse not only leads to serious drug dependence, but also produces irreversible neurotoxicity. Currently, there are no approved pharmacotherapies for the treatment of METH use disorders. Cannabidiol (CBD), a major non-psychoactive (and non-addictive) cannabinoid from the cannabis plant, shows neuroprotective, antioxidative, and anti-inflammatory properties under METH exposure. At present, however, the mechanisms underlying these properties remain unclear, which continues to hinder research on its therapeutic potential. In the current study, computational simulations showed that CBD and METH may directly bind to the dopamine receptor D1 (DRD1) via two overlapping binding sites. Moreover, CBD may compete with METH for the PHE-313 binding site. We also found that METH robustly induced apoptosis with activation of the caspase-8/caspase-3 cascade in-vitro and in-vivo, while CBD pretreatment prevented these changes. Furthermore, METH increased the expression of DRD1, phosphorylation of Methyl-CpG-binding protein 2 (MeCP2) at serine 421 (Ser421), and level of intracellular Ca2+in-vitro and in-vivo, but these effects were blocked by CBD pretreatment. The DRD1 antagonist SCH23390 significantly prevented METH-induced apoptosis, MeCP2 phosphorylation, and Ca2+ overload in-vitro. In contrast, the DRD1 agonist SKF81297 markedly increased apoptosis, MeCP2 phosphorylation, and Ca2+ overload, which were blocked by CBD pretreatment in-vitro. These results indicate that CBD prevents METH-induced neurotoxicity by modulating DRD1-mediated phosphorylation of MeCP2 and Ca2+ signaling. This study suggests that CBD pretreatment may resist the effects of METH on DRD1 by competitive binding.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Cannabidiol Prevented Growth Inhibition and Stereotyped Beha...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cannabidiol prevents methamphetamine-induced neurotoxicity by modulating dopamine receptor D1-mediated calcium-dependent phosphorylation of methyl-CpG-binding protein 2

et al. 2022

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Impact of cannabidiol on brain glucose metabolism of C57Bl/6 male mice previously exposed to cocaine

Spelta,

Real,

Bruno

et al. 2024

J of Neuroscience Research

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Despite evidence of the beneficial effects of cannabidiol (CBD) in animal models of cocaine use disorder (CUD), CBD neuronal mechanisms remain poorly understood. This study investigated the effects of CBD treatment on brain glucose metabolism, in a CUD animal model, using [18F]FDG positron emission tomography (PET). Male C57Bl/6 mice were injected with cocaine (20 mg/kg, i.p.) every other day for 9 days, followed by 8 days of CBD administration (30 mg/kg, i.p.). After 48 h, animals were challenged with cocaine. Control animals received saline/vehicle. [18F]FDG PET was performed at four time points: baseline, last day of sensitization, last day of withdrawal/CBD treatment, and challenge. Subsequently, the animals were euthanized and immunohistochemistry was performed on the hippocampus and amygdala to assess the CB1 receptors, neuronal nuclear protein, microglia (Iba1), and astrocytes (GFAP). Results showed that cocaine administration increased [18F]FDG uptake following sensitization. CBD treatment also increased [18F]FDG uptake in both saline and cocaine groups. However, animals that were sensitized and challenged with cocaine, and those receiving only an acute cocaine injection during the challenge phase, did not exhibit increased [18F]FDG uptake when treated with CBD. Furthermore, CBD induced modifications in the integrated density of NeuN, Iba, GFAP, and CB1R in the hippocampus and amygdala. This is the first study addressing the impact of CBD on brain glucose metabolism in a preclinical model of CUD using PET. Our findings suggest that CBD disrupts cocaine‐induced changes in brain energy consumption and activity, which might be correlated with alterations in neuronal and glial function.

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Cannabidiol inhibits methamphetamine-induced dopamine release via modulation of the DRD1-MeCP2-BDNF-TrkB signaling pathway

et al. 2022

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Cannabidiol promotes neurogenesis in the dentate gyrus during an abstinence period in rats following chronic exposure to methamphetamine

Cited by 7 publications

References 67 publications

Cannabidiol prevents methamphetamine-induced neurotoxicity by modulating dopamine receptor D1-mediated calcium-dependent phosphorylation of methyl-CpG-binding protein 2

Cannabidiol prevents methamphetamine-induced neurotoxicity by modulating dopamine receptor D1-mediated calcium-dependent phosphorylation of methyl-CpG-binding protein 2

Impact of cannabidiol on brain glucose metabolism of C57Bl/6 male mice previously exposed to cocaine

Cannabidiol inhibits methamphetamine-induced dopamine release via modulation of the DRD1-MeCP2-BDNF-TrkB signaling pathway

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