ArticleFrontiers in cellular neuroscience2015
Pharmacological blockade of the fatty acid amide hydrolase (FAAH) alters neural proliferation, apoptosis and gliosis in the rat hippocampus, hypothalamus and striatum in a negative energy context.
Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 49 citations in OpenAlex.
- Photoreceptor preservation by FAAH inhibition in a murine model of retinitis pigmentosa.Molecular neurobiology · 2026Article
- Environmental pollutants and autism spectrum disorder: Effects of plasticizers on core phenotypes and molecular targets.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Chronic suppression of monoacylglycerol lipase restores adult neurogenesis in the septal but not the temporal DG in Ts65Dn mouse model of Down syndrome.Brain research bulletin · 2026Article
- Article
- Interplays of Dietary Fat with BMI andFood science & nutrition · 2024Article
- Inhibition of Adult Neurogenesis in Male Mice after Repeated Exposure to Paracetamol Overdose.International journal of molecular sciences · 2024Article
- Effect of MCH1, a fatty-acid amide hydrolase inhibitor, on the depressive-like behavior and gene expression of endocannabinoid and dopaminergic-signaling system in the mouse nucleus accumbens.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024Article
- Identification of brain areas in mice with peak neural activity across the acute and persistent phases of post-traumatic headache.Cephalalgia : an international journal of headache · 2023Article
- Fit-for-purpose based testing and validation of antibodies to amino- and carboxy-terminal domains of cannabinoid receptor 1.Histochemistry and cell biology · 2021Article
- Early Consumption of Cannabinoids: From Adult Neurogenesis to Behavior.International journal of molecular sciences · 2021Review
- Experimental Activation of Endocannabinoid System Reveals Antilipotoxic Effects on Cardiac Myocytes.Molecules (Basel, Switzerland) · 2020Article
- Cannabinoid Actions on Neural Stem Cells: Implications for Pathophysiology.Molecules (Basel, Switzerland) · 2019Review
- Modulation of Cognition: The Role ofNeural plasticity · 2019Article
- Oleoylethanolamide Modulates BDNF-ERK Signaling and Neurogenesis in the Hippocampi of Rats Exposed to ΔFrontiers in molecular neuroscience · 2019Article
- 2-Pentadecyl-2-Oxazoline Reduces Neuroinflammatory Environment in the MPTP Model of Parkinson Disease.Molecular neurobiology · 2018Article
- Inhibition of Fatty Acid Amide Hydrolase by PF-3845 Alleviates the Nitrergic and Proinflammatory Response in Rat Hippocampus Following Acute Stress.The international journal of neuropsychopharmacology · 2018Article
- Palmitoylethanolamide Ameliorates Hippocampal Damage and Behavioral Dysfunction After Perinatal Asphyxia in the Immature Rat Brain.Frontiers in neuroscience · 2018Article
- Antiepileptogenic Effect of Subchronic Palmitoylethanolamide Treatment in a Mouse Model of Acute Epilepsy.Frontiers in molecular neuroscience · 2018Article
- Environmental Enrichment, Age, and PPARα Interact to Regulate Proliferation in Neurogenic Niches.Frontiers in neuroscience · 2016Article
- Pharmacological activation of CB2 receptors counteracts the deleterious effect of ethanol on cell proliferation in the main neurogenic zones of the adult rat brain.Frontiers in cellular neuroscience · 2015Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endocannabinoids participate in the control of neurogenesis, neural cell death and gliosis. The pharmacological effect of the fatty acid amide hydrolase (FAAH) inhibitor URB597, which limits the endocannabinoid degradation, was investigated in the present study. Cell proliferation (phospho-H3(+) or BrdU(+) cells) of the main adult neurogenic zones as well as apoptosis (cleaved caspase-3(+)), astroglia (GFAP(+)), and microglia (Iba1(+) cells) were analyzed in the hippocampus, hypothalamus and striatum of rats intraperitoneally treated with URB597 (0.3 mg/kg/day) at one dose/4-days resting or 5 doses (1 dose/day). Repeated URB597 treatment increased the plasma levels of the N-acylethanolamines oleoylethanolamide, palmitoylethanolamide and arachidonoylethanolamine, reduced the plasma levels of glucose, triglycerides and cholesterol, and induced a transitory body weight decrease. The hippocampi of repeated URB597-treated rats showed a reduced number of phospho-H3(+) and BrdU(+) subgranular cells as well as GFAP(+), Iba1(+) and cleaved caspase-3(+) cells, which was accompanied with decreased hippocampal expression of the cannabinoid CB1 receptor gene Cnr1 and Faah. In the hypothalami of these rats, the number of phospho-H3(+), GFAP(+) and 3-weeks-old BrdU(+) cells was specifically decreased. The reduced striatal expression of CB1 receptor in repeated URB597-treated rats was only associated with a reduced apoptosis. In contrast, the striatum of acute URB597-treated rats showed an increased number of subventricular proliferative, astroglial and apoptotic cells, which was accompanied with increased Faah expression. Main results indicated that FAAH inhibitor URB597 decreased neural proliferation, glia and apoptosis in a brain region-dependent manner, which were coupled to local changes in Faah and/or Cnr1 expression and a negative energy context.
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