Anandamide Reduces the Toxic Synergism Exerted by Quinolinic Acid and Glutaric Acid in Rat Brain Neuronal Cells

Kotlar, Ilan; Rangel-López, Edgar; Colonnello, Aline; Aguilera-Portillo, Gabriela; Serratos, Iris N.; Galván‐Arzate, Sonia; Pedraza‐Chaverrí, José; Túnez, Isaac; Wajner, Moaçir; Santamarı́a, Abel

doi:10.1016/j.neuroscience.2019.01.014

Cited by 11 publications

(5 citation statements)

References 56 publications

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“…The levels of protection displayed by these agents for different toxic endpoints suggest their broad spectrum of neuromodulatory actions at different cell levels. Neuroprotective effects of endocannabinoids, synthetic cannabinoids, and the inhibitor of FAAH, URB597, have been recently reported in other toxic models combining excitotoxicity and oxidative damage (Rangel-López et al, 2015;Aguilera-Portillo et al, 2019;Maya-López et al, 2019;Kotlar et al, 2019).…”

Section: Discussionmentioning

confidence: 95%

Cannabinoid-profiled agents improve cell survival via reduction of oxidative stress and inflammation, and Nrf2 activation in a toxic model combining hyperglycemia+Aβ1-42 peptide in rat hippocampal neurons

Elmazoğlu

Rangel-López

Medina-Campos

et al. 2020

Neurochemistry International

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Section: Discussionmentioning

confidence: 95%

Cannabinoid-profiled agents improve cell survival via reduction of oxidative stress and inflammation, and Nrf2 activation in a toxic model combining hyperglycemia+Aβ1-42 peptide in rat hippocampal neurons

Elmazoğlu

Rangel-López

Medina-Campos

et al. 2020

Neurochemistry International

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“…A further study showed that QA enhanced CD3 staining and the number of YNO2 positive cells in these animals, implying T lymphocyte infiltration and nitrosative stress, respectively (Amaral et al, 2018). Synergistic toxic effects of QA and GA in neuronal cultures, co‐cultures and mixed cultures from WT rat cerebral cortex and striatum has been also recently described, strengthening a synergistic role of QA and GA in GA I neurodegeneration (Pierozan et al, 2018; Kotlar et al, 2019). Taken together, these observations support the hypothesis that QA may potentially contribute to GA I neuropathogenesis, as originally proposed (Varadkar and Surtees, 2004).…”

Section: Oxidative Stress and Neuroinflammation In Gcdh−/− Micementioning

confidence: 84%

Pathogenesis of brain damage in glutaric acidemia type I: Lessons from the genetic mice model

Wajner

Amaral

Leipnitz

2019

Intl J of Devlp Neuroscience

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Glutaric acidemia type I (GA I) is an inherited neurometabolic disease caused by deficient activity of the mitochondrial enzyme glutaryl‐CoA dehydrogenase (GCDH), resulting in predominant accumulation of glutaric and 3‐hydroxyglutaric acids derived from lysine (Lys), hydroxylysine, and tryptophan catabolism. GA I patients usually present progressive cortical leukodystrophy and frequently develop acute striatal degeneration during encephalopathic crises during the first three years of life. The pathophysiology of the neurodegeneration observed in GA I is still partly known, although the development of the genetic mice model of GA I (Gcdh−/−) has contributed to clarify potential underlying mechanisms involved in brain damage in this disease. In this review we will summarize the knowledge acquired from studies using this animal model indicating that disruption of redox homeostasis, glutamatergic neurotransmission and bioenergetics, as well as vascular alterations, blood‐brain barrier breakage and altered myelination underlie the cortical and striatum abnormalities and white matter changes observed in GA I patients. Elucidation of these pathomechanisms potentially offers new standpoints for the development of novel therapeutic strategies for this disease.

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“…Several lines of evidence have shown that TRPV1 activation by CAP produces anandamide (AEA), which activates TRPV1 and/or the CB receptor [ 15 , 24 , 25 ] and prevents neurodegeneration in vivo and in vitro [ 16 , 26 – 28 ]. Accordingly, we determined whether AEA, when exogenously administered, could rescue nigrostriatal dopamine neurons.…”

Section: Resultsmentioning

confidence: 99%

Functional Crosstalk between CB and TRPV1 Receptors Protects Nigrostriatal Dopaminergic Neurons in the MPTP Model of Parkinson’s Disease

Chung

Jin

2020

Journal of Immunology Research

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The present study examined whether crosstalk between cannabinoid (CB) and transient potential receptor vanilloid type 1 (TRPV1) could contribute to the survival of nigrostriatal dopamine neurons in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson’s disease (PD). MPTP induced a significant loss of nigrostriatal dopamine neurons and glial activation in the substantia nigra (SN) and striatum (STR) as visualized by tyrosine hydroxylase (TH) or macrophage antigen complex-1 (MAC-1) or glial fibrillary acidic protein (GFAP) immunocytochemistry, respectively. RT-PCR analysis shows the upregulation of inducible nitric oxide synthase, interleukin-1β, and tumor necrosis factor-α in microglia in the SN in vivo, indicating the activation of the inflammatory system. By contrast, treatment with capsaicin (a specific TRPV1 agonist) increased the survival of dopamine neurons in the SN and their fibers and dopamine levels in the STR in MPTP mice. Capsaicin neuroprotection is accompanied by inhibiting MPTP-induced glial activation and production of inflammatory cytokines. Treatment with AM251 and AM630 (CB1/2 antagonists) abolished capsaicin-induced beneficial effects, indicating the existence of a functional crosstalk between CB and TRPV1. Moreover, treatment with anandamide (an endogenous agonist for both CB and TRVP1) rescued nigrostriatal dopamine neurons and reduced gliosis-derived neuroinflammatory responses in MPTP mice. These results suggest that the cannabinoid and vanilloid system may be beneficial for the treatment of neurodegenerative diseases, such as PD, that are associated with neuroinflammation.

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Anandamide Reduces the Toxic Synergism Exerted by Quinolinic Acid and Glutaric Acid in Rat Brain Neuronal Cells

Cited by 11 publications

References 56 publications

Cannabinoid-profiled agents improve cell survival via reduction of oxidative stress and inflammation, and Nrf2 activation in a toxic model combining hyperglycemia+Aβ1-42 peptide in rat hippocampal neurons

Cannabinoid-profiled agents improve cell survival via reduction of oxidative stress and inflammation, and Nrf2 activation in a toxic model combining hyperglycemia+Aβ1-42 peptide in rat hippocampal neurons

Pathogenesis of brain damage in glutaric acidemia type I: Lessons from the genetic mice model

Functional Crosstalk between CB and TRPV1 Receptors Protects Nigrostriatal Dopaminergic Neurons in the MPTP Model of Parkinson’s Disease

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