ArticleBiological psychiatry2015
Chronic cannabinoid receptor 2 activation reverses paclitaxel neuropathy without tolerance or cannabinoid receptor 1-dependent withdrawal.
Article in Biological psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.
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Who cites it
123 citing papers in PubMed.
- Cannabinoid CBBritish journal of pharmacology · 2026Article
- Cannabidiol attenuates chemotherapy-induced peripheral neuropathic pain through a mechanism that requires the enzymebioRxiv : the preprint server for biology · 2026Article
- Endocannabinoid system modulation in acute, chronic, and neuropathic pain: reviewing experimental models, clinical evidence, and nanotechnology delivery.Metabolic brain disease · 2026Review
- Cannabinoid efficacy for pain: dose, chronicity and route.Frontiers in neuroscience · 2026Review
- CB2 cannabinoid receptor-specific therapeutic antibody agonists for treatment of chemotherapy-induced peripheral neuropathy.bioRxiv : the preprint server for biology · 2025Article
- Activation of µ-δ Opioid Receptor Heteromer Attenuates Chemotherapy-Induced Neuropathic Pain in Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Cannabinoid CBBritish journal of pharmacology · 2025Review
- Breast Cancer Cell Lines AT-3 and E0771 Decrease Mechanical and Cold Sensitivity, Along With Oestrous Cycle and Inflammatory Marker Alterations, in Wild-Type C57BL/6J Female Mice.European journal of pain (London, England) · 2025Article
- CB1 and CB2 receptors differentially modulate the cognitive impact of maternal immune activation and perinatal cannabinoid exposure.Behavioural brain research · 2025Article
- The cannabinoid CBNeuropharmacology · 2025Article
- ART26.12, a novel fatty acid-binding protein 5 inhibitor, shows efficacy in multiple preclinical neuropathy models.European journal of pain (London, England) · 2025Article
- Chronic Administration of Cannabinoid Agonists ACEA, AM1241, and CP55,940 Induce Sex-Specific Differences in Tolerance and Sex Hormone Changes in a Chemotherapy-Induced Peripheral Neuropathy.The Journal of pharmacology and experimental therapeutics · 2024Article
- Chemotherapy-Induced Peripheral Neuropathy: A Recent Update on Pathophysiology and Treatment.Life (Basel, Switzerland) · 2024Review
- Cannabinoid CBBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Article
- Discovery and Preclinical Evaluation of a Novel Inhibitor of FABP5, ART26.12, Effective in Oxaliplatin-Induced Peripheral Neuropathy.The journal of pain · 2024Article
- The effect of cannabinoid type 2 receptor agonist on morphine tolerance.IBRO neuroscience reports · 2024Review
- Tetrahydrocannabinol and Cannabidiol for Pain Treatment-An Update on the Evidence.Biomedicines · 2024Review
- Article
- The potential neuroprotective effects of cannabinoids against paclitaxel-induced peripheral neuropathy:Frontiers in pharmacology · 2024Article
- A monoacylglycerol lipase inhibitor showing therapeutic efficacy in mice without central side effects or dependence.Nature communications · 2023Article
63 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundMixed cannabinoid receptor 1 and 2 (CB1 and CB2) agonists such as Δ(9)-tetrahydrocannabinol (Δ(9)-THC) can produce tolerance, physical withdrawal, and unwanted CB1-mediated central nervous system side effects. Whether repeated systemic administration of a CB2-preferring agonist engages CB1 receptors or produces CB1-mediated side effects is unknown.
methodsWe evaluated antiallodynic efficacy, possible tolerance, and cannabimimetic side effects of repeated dosing with a CB2-preferring agonist AM1710 in a model of chemotherapy-induced neuropathy produced by paclitaxel using CB1 knockout (CB1KO), CB2 knockout (CB2KO), and wild-type (WT) mice. Comparisons were made with the prototypic classic cannabinoid Δ(9)-THC. We also explored the site and possible mechanism of action of AM1710.
resultsPaclitaxel-induced mechanical and cold allodynia developed to an equivalent degree in CB1KO, CB2KO, and WT mice. Both AM1710 and Δ(9)-THC suppressed established paclitaxel-induced allodynia in WT mice. In contrast to Δ(9)-THC, chronic administration of AM1710 did not engage CB1 activity or produce antinociceptive tolerance, CB1-mediated cannabinoid withdrawal, hypothermia, or motor dysfunction. Antiallodynic efficacy of systemic administration of AM1710 was absent in CB2KO mice and WT mice receiving the CB2 antagonist AM630, administered either systemically or intrathecally. Intrathecal administration of AM1710 also attenuated paclitaxel-induced allodynia in WT mice, but not CB2KO mice, implicating a possible role for spinal CB2 receptors in AM1710 antiallodynic efficacy. Finally, both acute and chronic administration of AM1710 decreased messenger RNA levels of tumor necrosis factor-α and monocyte chemoattractant protein 1 in lumbar spinal cord of paclitaxel-treated WT mice.
conclusionsOur results highlight the potential of prolonged use of CB2 agonists for managing chemotherapy-induced allodynia with a favorable therapeutic ratio marked by sustained efficacy and absence of tolerance, physical withdrawal, or CB1-mediated side effects.
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