ArticlePsychopharmacology2011
AVE1625, a cannabinoid CB1 receptor antagonist, as a co-treatment with antipsychotics for schizophrenia: improvement in cognitive function and reduction of antipsychotic-side effects in rodents.
Article in Psychopharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.
- Cannabinoid Receptors: An Update on Cell Signaling, Pathophysiological Roles and Therapeutic Opportunities in Neurological, Cardiovascular, and Inflammatory Diseases.International journal of molecular sciences · 2020Pooled it
- Auditory evoked-potential abnormalities in a mouse model of 22q11.2 Deletion Syndrome and their interactions with hearing impairment.Translational psychiatry · 2025Article
- Anxiety Modulation by Cannabinoids-The Role of Stress Responses and Coping.International journal of molecular sciences · 2023Review
- Structural and functional insights into the G protein-coupled receptors: CB1 and CB2.Biochemical Society transactions · 2023Review
- Gene, cell type, and drug prioritization analysis suggest genetic basis for the utility of diuretics in treating Alzheimer disease.HGG advances · 2023Article
- Mechanism and treatments of antipsychotic-induced weight gain.International journal of obesity (2005) · 2023Review
- Molecular Alterations of the Endocannabinoid System in Psychiatric Disorders.International journal of molecular sciences · 2022Review
- Why Do Marijuana and Synthetic Cannabimimetics Induce Acute Myocardial Infarction in Healthy Young People?Cells · 2022Review
- Molecular Targets of Cannabinoids Associated with Depression.Current medicinal chemistry · 2022Review
- Obesity as a Condition Determined by Food Addiction: Should Brain Endocannabinoid System Alterations Be the Cause and Its Modulation the Solution?Pharmaceuticals (Basel, Switzerland) · 2021Review
- Endocannabinoid System Components as Potential Biomarkers in Psychiatry.Frontiers in psychiatry · 2020Review
- Probing the CBMolecular pharmacology · 2019Article
- Role of the Endocannabinoid System in the Pathophysiology of Schizophrenia.Molecular neurobiology · 2017Review
- Cannabinoid antagonist SLV326 induces convulsive seizures and changes in the interictal EEG in rats.PloS one · 2017Article
- Article
- Endocannabinoid control of glutamate NMDA receptors: the therapeutic potential and consequences of dysfunction.Oncotarget · 2016Review
- The phytocannabinoid, Δ⁹-tetrahydrocannabivarin, can act through 5-HT₁A receptors to produce antipsychotic effects.British journal of pharmacology · 2015Article
- Endocannabinoids and the Endocrine System in Health and Disease.Handbook of experimental pharmacology · 2015Review
- CB2 receptor agonism reverses MK-801-induced disruptions of prepulse inhibition in mice.Psychopharmacology · 2014Article
- Effects of cannabinoid drugs on the deficit of prepulse inhibition of startle in an animal model of schizophrenia: the SHR strain.Frontiers in pharmacology · 2014Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleThe psychotomimetic effects of cannabis are believed to be mediated via cannabinoid CB1 receptors. Furthermore, studies have implicated CB1 receptors in the pathophysiology of schizophrenia.
objectiveThese studies investigated the effects of the CB1 receptor antagonist, AVE1625, in acute pharmacological and neurodevelopmental models of schizophrenia. AVE1625 was administered to rodents alone or as a co-treatment with clinically used antipsychotic drugs (APDs).
methodsThe antipsychotic potential of AVE1625 was tested using psychotomimetic-induced hyperactivity and latent inhibition (LI) deficit models. The procognitive profile was assessed using hole board, novel object recognition, auditory evoked potential, and LI techniques. In addition, the side-effect profile was established by measuring catalepsy, antipsychotic-induced weight gain, plasma levels of prolactin, and anxiogenic potential.
resultsAVE1625 (1, 3, and 10 mg/kg ip), reversed abnormally persistent LI induced by MK-801 or neonatal nitric oxide synthase inhibition in rodents, and improved both working and episodic memory. AVE1625 was not active in positive symptom models but importantly, it did not diminish the efficacy of APDs. It also decreased catalepsy and weight gain induced by APDs, suggesting that it may decrease APD-induced extrapyramidal side effects (EPS) and compliance. Unlike other CB1 antagonists, AVE1625 did not produce anxiogenic-like effects.
conclusionsThese preclinical data suggest that AVE1625 may be useful to treat the cognitive deficits in schizophrenia and as a co-treatment with currently available antipsychotics. In addition, an improved side-effect profile was seen, with potential to ameliorate the EPS and weight gain issues with currently available treatments.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.