The Endocannabinoid, Anandamide, Augments Notch-1 Signaling in Cultured Cortical Neurons Exposed to Amyloid-β and in the Cortex of Aged Rats

Tanveer, Riffat; Gowran, Aoife; Noonan, Janis; Keating, Sinéad E.; Bowie, Andrew; Campbell, Veronica A.

doi:10.1074/jbc.m112.350678

Cited by 46 publications

(42 citation statements)

References 62 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We observed that CB1R activation did not induce differentiation of GFAP-positive astrocytes or Olig2-positive oligodendrocytes. However, previous published results are apparently discordant because some authors have shown that endocannabinoid treatment promotes astroglial and/or oligodendroglial differentiation [38], [41], [46], [47] while others have shown that CB1R activation promotes neuronal differentiation [40], [48]. Our results are in accordance with an effect mediated by CB1R activation on neuronal differentiation.…”

Section: Discussionsupporting

confidence: 60%

“…In addition, we observed that inhibiting the Notch pathway with DAPT blocked the increase in self-renewal induced by R-m-AEA treatment, suggesting that the notch pathway mediates CB1R induction of self-renewal. In fact, Tanveer and collaborators [41] have shown that anandamide, increases Notch-1 signaling in cortical neurons exposed to amyloid-beta and in the cortex of aged rats.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Activation of Type 1 Cannabinoid Receptor (CB1R) Promotes Neurogenesis in Murine Subventricular Zone Cell Cultures

et al. 2013

View full text Add to dashboard Cite

The endocannabinoid system has been implicated in the modulation of adult neurogenesis. Here, we describe the effect of type 1 cannabinoid receptor (CB1R) activation on self-renewal, proliferation and neuronal differentiation in mouse neonatal subventricular zone (SVZ) stem/progenitor cell cultures. Expression of CB1R was detected in SVZ-derived immature cells (Nestin-positive), neurons and astrocytes. Stimulation of the CB1R by (R)-(+)-Methanandamide (R-m-AEA) increased self-renewal of SVZ cells, as assessed by counting the number of secondary neurospheres and the number of Sox2+/+ cell pairs, an effect blocked by Notch pathway inhibition. Moreover, R-m-AEA treatment for 48 h, increased proliferation as assessed by BrdU incorporation assay, an effect mediated by activation of MAPK-ERK and AKT pathways. Surprisingly, stimulation of CB1R by R-m-AEA also promoted neuronal differentiation (without affecting glial differentiation), at 7 days, as shown by counting the number of NeuN-positive neurons in the cultures. Moreover, by monitoring intracellular calcium concentrations ([Ca2+]i) in single cells following KCl and histamine stimuli, a method that allows the functional evaluation of neuronal differentiation, we observed an increase in neuronal-like cells. This proneurogenic effect was blocked when SVZ cells were co-incubated with R-m-AEA and the CB1R antagonist AM 251, for 7 days, thus indicating that this effect involves CB1R activation. In accordance with an effect on neuronal differentiation and maturation, R-m-AEA also increased neurite growth, as evaluated by quantifying and measuring the number of MAP2-positive processes. Taken together, these results demonstrate that CB1R activation induces proliferation, self-renewal and neuronal differentiation from mouse neonatal SVZ cell cultures.

show abstract

Section: Discussionsupporting

confidence: 60%

Section: Discussionmentioning

confidence: 99%

Activation of Type 1 Cannabinoid Receptor (CB1R) Promotes Neurogenesis in Murine Subventricular Zone Cell Cultures

et al. 2013

View full text Add to dashboard Cite

show abstract

“…In another study (Tanveer et al . ), it was reported that AEA up‐regulates Notch‐1 signaling in cultured neurons. Exposure of cultured neurons to Aβ (1‐42) increases expression of the endogenous inhibitor of Notch‐1, numb (Nb), leading to impaired Notch‐1 signaling.…”

Section: Changes In the Endocannabinoid System In Neurodegenerative Dmentioning

confidence: 96%

Endocannabinoid system in neurodegenerative disorders

Basavarajappa

Shivakumar

Joshi

et al. 2017

Journal of Neurochemistry

161

140

View full text Add to dashboard Cite

Most neurodegenerative disorders (NDDs) are characterized by cognitive impairment and other neurological defects. The definite cause of and pathways underlying the progression of these NDDs are not well defined. Several mechanisms have been proposed to contribute to the development of NDDs. These mechanisms may proceed concurrently or successively, and they differ among cell types at different developmental stages in distinct brain regions. The endocannabinoid system, which involves cannabinoid receptors type 1 (CB1R) and type 2 (CB2R), endogenous cannabinoids and the enzymes that catabolize these compounds, has been shown to contribute to the development of NDDs in several animal models and human studies. In this review, we discuss the functions of the endocannabinoid (EC) system in NDDs and converse the therapeutic efficacy of targeting the endocannabinoid system to rescue NDDs.

show abstract

“…AEA might offer neuroprotection of neurodegeneration. Enhancement of AEA might enhance Notch signaling and could provide a therapy to ease symptoms and hold off progression of neurodegeneration (Khaspekov, 2004;Ramírez, 2005;Tanveer, 2012).…”

Section: Figmentioning

confidence: 99%

Metabolic Biomarkers and Neurodegeneration: A Pathway Enrichment Analysis of Alzheimer's Disease, Parkinson's Disease, and Amyotrophic Lateral Sclerosis

Kori

Aydın

Unal

et al. 2016

OMICS: A Journal of Integrative Biology

122

View full text Add to dashboard Cite

Neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS) lack robust diagnostics and prognostic biomarkers. Metabolomics is a postgenomics field that offers fresh insights for biomarkers of common complex as well as rare diseases. Using data on metabolite-disease associations published in the previous decade (2006-2016) in PubMed, ScienceDirect, Scopus, and Web of Science, we identified 101 metabolites as putative biomarkers for these three neurodegenerative diseases. Notably, uric acid, choline, creatine, L-glutamine, alanine, creatinine, and N-acetyl-L-aspartate were the shared metabolite signatures among the three diseases. The disease-metabolite-pathway associations pointed out the importance of membrane transport (through ATP binding cassette transporters), particularly of arginine and proline amino acids in all three neurodegenerative diseases. When disease-specific and common metabolic pathways were queried by using the pathway enrichment analyses, we found that alanine, aspartate, glutamate, and purine metabolism might act as alternative pathways to overcome inadequate glucose supply and energy crisis in neurodegeneration. These observations underscore the importance of metabolite-based biomarker research in deciphering the elusive pathophysiology of neurodegenerative diseases. Future research investments in metabolomics of complex diseases might provide new insights on AD, PD, and ALS that continue to place a significant burden on global health.

show abstract

The Endocannabinoid, Anandamide, Augments Notch-1 Signaling in Cultured Cortical Neurons Exposed to Amyloid-β and in the Cortex of Aged Rats

Cited by 46 publications

References 62 publications

Activation of Type 1 Cannabinoid Receptor (CB1R) Promotes Neurogenesis in Murine Subventricular Zone Cell Cultures

Activation of Type 1 Cannabinoid Receptor (CB1R) Promotes Neurogenesis in Murine Subventricular Zone Cell Cultures

Endocannabinoid system in neurodegenerative disorders

Metabolic Biomarkers and Neurodegeneration: A Pathway Enrichment Analysis of Alzheimer's Disease, Parkinson's Disease, and Amyotrophic Lateral Sclerosis

Contact Info

Product

Resources

About