Cannabinoid-induced actomyosin contractility shapes neuronal morphology and growth

Roland, Alexandre B.; Ricobaraza, Ana; Carrel, Damien; Jordan, Benjamin M; Rico, Félix; Simon, Anne; Humbert-Claude, Marie; Ferrier, Jérémy; McFadden, Maureen H; Scheuring, Simon; Lenkei, Zsolt

doi:10.7554/elife.03159

Cited by 85 publications

(104 citation statements)

References 55 publications

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“…To our knowledge, this is the first study reporting that WIN55212-2 signals through Gα 12/13 in brain cortex. These data are concordant with other studies suggesting that cannabinoids induce the stimulation of this RhoA-activator (Dalton et al, 2013; Roland et al, 2014). Moreover, our results from knockout mice show that the WIN55212-2-induced signaling through Gα 12/13 in the brain seems to be mediated, mainly, by the CB 2 receptor.…”

Section: Discussionsupporting

confidence: 93%

Biased Agonism of Three Different Cannabinoid Receptor Agonists in Mouse Brain Cortex

et al. 2016

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Cannabinoid receptors are able to couple to different families of G proteins when activated by an agonist drug. It has been suggested that different intracellular responses may be activated depending on the ligand. The goal of the present study was to characterize the pattern of G protein subunit stimulation triggered by three different cannabinoid ligands, Δ9-THC, WIN55212-2, and ACEA in mouse brain cortex. Stimulation of the [35S]GTPγS binding coupled to specific immunoprecipitation with antibodies against different subtypes of G proteins (Gαi1, Gαi2, Gαi3, Gαo, Gαz, Gαs, Gαq/11, and Gα12/13), in the presence of Δ9-THC, WIN55212-2 and ACEA (submaximal concentration 10 μM) was determined by scintillation proximity assay (SPA) technique in mouse cortex of wild type, CB1 knock-out, CB2 knock-out and CB1/CB2 double knock-out mice. Results show that, in mouse brain cortex, cannabinoid agonists are able to significantly stimulate not only the classical inhibitory Gαi/o subunits but also other G subunits like Gαz, Gαq/11, and Gα12/13. Moreover, the specific pattern of G protein subunit activation is different depending on the ligand. In conclusion, our results demonstrate that, in mice brain native tissue, different exogenous cannabinoid ligands are able to selectively activate different inhibitory and non-inhibitory Gα protein subtypes, through the activation of CB1 and/or CB2 receptors. Results of the present study may help to understand the specific molecular pathways involved in the pharmacological effects of cannabinoid-derived drugs.

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Section: Discussionsupporting

confidence: 93%

Biased Agonism of Three Different Cannabinoid Receptor Agonists in Mouse Brain Cortex

et al. 2016

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“…This raises the possibility that the CB 1 R promotes lppLTP via actions on actin regulatory signaling, an idea in alignment with evidence that CB 1 R initiates actin reorganization in dissociated cells (Roland et al 2014;Njoo et al 2015) and rapidly (~2 min) activates both FAK and the small GTPase RhoA in N18TG2 neuroblastoma cells (Dalton et al 2013). FAK is a non-receptor tyrosine kinase that mediates integrin effects on the actin cytoskeleton throughout the body (Fabry et al 2011).…”

Section: Cb 1 R Signaling In Lpp Terminalsmentioning

confidence: 70%

Atypical Endocannabinoid Signaling Initiates a New Form of Memory-Related Plasticity at a Cortical Input to Hippocampus

et al. 2017

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Endocannabinoids (ECBs) depress transmitter release at sites throughout the brain. Here, we describe another form of ECB signaling that triggers a novel form of long-term potentiation (LTP) localized to the lateral perforant path (LPP) which conveys semantic information from cortex to hippocampus. Two cannabinoid CB 1 receptor (CB 1 R) signaling cascades were identified in hippocampus. The first is pregnenolone sensitive, targets vesicular protein Munc18-1 and depresses transmitter release; this cascade is engaged by CB 1 Rs in Schaffer-Commissural afferents to CA1 but not in the LPP, and it does not contribute to LTP. The second cascade is pregnenolone insensitive and LPP specific; it entails co-operative CB 1 R/β1-integrin signaling to effect synaptic potentiation via stable enhancement of transmitter release. The latter cascade is engaged during LPP-dependent learning. These results link atypical ECB signaling to the encoding of a fundamental component of episodic memory and suggest a novel route whereby endogenous and exogenous cannabinoids affect cognition.

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“…As mentioned in this chapter, PUFA accretion in the brain occurs largely during brain development and our laboratory published many articles on the effects of imbalanced dietary PUFA during development on the adult brain [3,7,26]. In parallel, increasing evidence highlights that endocannabinoid signaling is essential for brain wiring [170,171]. Notably, endocannabinoids and CB1 receptors serve as guidance signals for axon cone growth [171].…”

Section: Perspectives: Implications For Future Therapeutics Of Endocamentioning

confidence: 99%

“…In parallel, increasing evidence highlights that endocannabinoid signaling is essential for brain wiring [170,171]. Notably, endocannabinoids and CB1 receptors serve as guidance signals for axon cone growth [171]. The link between dietary PUFA and endocannabinoids is not yet clearly established, but it is very likely that effects of imbalanced PUFAs during development has strong consequences on the role of endocannabinoid as guidance molecules during brain wiring.…”

Section: Perspectives: Implications For Future Therapeutics Of Endocamentioning

confidence: 99%

Dietary Omega-6/Omega-3 and Endocannabinoids: Implications for Brain Health and Diseases

Bosch‐Bouju¹,

Layé²

2016

Cannabinoids in Health and Disease

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Omega-3 (ω-3) and omega-6 (ω-6) are polyunsaturated fatty acids (PUFAs) that play critical role in human health and have to be provided by food. In the brain, PUFAs are also precursors of endocannabinoids. The aim of this chapter is to review the existing literature on how dietary PUFAs impact on the endocannabinoid system in the brain and what are the consequences for brain function and dysfunction. In this chapter, we will first describe how PUFAs enter the brain, what are their metabolism processes and roles in brain function. We will describe the pathways from PUFAs to endocannabinoid production. Then, we will review the literature on how dietary ω-6/ω-3 ratio impacts the endocannabinoid system, in terms of endocannabinoid levels, proteins and endocannabinoid-dependent synaptic plasticity. In the next part, we will describe what we know about the interactions between PUFAs and endocannabinoids in neurological and neuropsychiatric disorders. Finally, we will conclude on the possible implications of the interactions between dietary PUFAs and endocannabinoids in the normal and pathological brain. In particular, we will discuss how dietary PUFAs, as homeostatic regulators of endocannabinoids, can constitute interesting therapeutic strategies for the prevention and/or treatment of neurological disorders with endocannabinoids impairment.

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Cannabinoid-induced actomyosin contractility shapes neuronal morphology and growth

Cited by 85 publications

References 55 publications

Biased Agonism of Three Different Cannabinoid Receptor Agonists in Mouse Brain Cortex

Biased Agonism of Three Different Cannabinoid Receptor Agonists in Mouse Brain Cortex

Atypical Endocannabinoid Signaling Initiates a New Form of Memory-Related Plasticity at a Cortical Input to Hippocampus

Dietary Omega-6/Omega-3 and Endocannabinoids: Implications for Brain Health and Diseases

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