Neuronal and astrocytic localization of the cannabinoid receptor-1 in the dorsal horn of the rat spinal cord

Salio, Chiara; Doly, Stéphane; Fischer, Jacqueline; Franzoni, Maria Fosca; Conrath, M.

doi:10.1016/s0304-3940(02)00549-9

Cited by 79 publications

(63 citation statements)

References 20 publications

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“…While evidence for CB 1 receptor expression by astrocytes has been found by some groups (Bouaboula et al, 1995;Sanchez et al, 1998;Moldrich & Wenger, 2000;Abood et al, 2001;Rodriguez et al, 2001;Molina-Holgado et al, 2002b;Salio et al, 2002), it has not been found by others (Sagan et al, 1999;Walter & Stella, 2003b). These conflicting results may indicate variations in CB 1 receptor expression due to differences in species, culture systems, CNS structures from which cultures are derived, ages of cultures, or activation levels of cells; CB 2 receptor expression by astrocytes has not been found (Walter & Stella, 2003b).…”

Section: Glial Cells Express Cannabinoid Receptorsmentioning

confidence: 97%

Cannabinoids and neuroinflammation

Walter

Stella

2004

British J Pharmacology

303

215

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Growing evidence suggests that a major physiological function of the cannabinoid signaling system is to modulate neuroinflammation. This review discusses the anti-inflammatory properties of cannabinoid compounds at molecular, cellular and whole animal levels, first by examining the evidence for anti-inflammatory effects of cannabinoids obtained using in vivo animal models of clinical neuroinflammatory conditions, specifically rodent models of multiple sclerosis, and second by describing the endogenous cannabinoid (endocannabinoid) system components in immune cells. Our aim is to identify immune functions modulated by cannabinoids that could account for their antiinflammatory effects in these animal models.

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Section: Glial Cells Express Cannabinoid Receptorsmentioning

confidence: 97%

Cannabinoids and neuroinflammation

Walter

Stella

2004

British J Pharmacology

303

215

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“…Earlier studies showed discrepancies in the expression of CB1Rs by astrocytes in culture (see [30]), which could arise from the well-known phenotypic changes in astrocytes in different culture conditions. Indeed, several studies indicated the presence of such changes in astrocytes in culture and in situ [30][31][32][33][34][35] This activation increased astrocyte Ca 2þ levels through the mobilization of Ca 2þ from internal stores [9]. The intracellular signalling pathway underlying this effect exhibited specific characteristics.…”

Section: Endocannabinoid Signalling In Neuronastrocyte Communicationmentioning

confidence: 99%

Astrocytes in endocannabinoid signalling

Navarrete

Díez

Araque

2014

Phil. Trans. R. Soc. B

112

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Astrocytes are emerging as integral functional components of synapses, responding to synaptically released neurotransmitters and regulating synaptic transmission and plasticity. Thus, they functionally interact with neurons establishing tripartite synapses: a functional concept that refers to the existence of communication between astrocytes and neurons and its crucial role in synaptic function. Here, we discuss recent evidence showing that astrocytes are involved in the endocannabinoid (ECB) system, responding to exogenous cannabinoids as well as ECBs through activation of type 1 cannabinoid receptors, which increase intracellular calcium and stimulate the release of glutamate that modulates synaptic transmission and plasticity. We also discuss the consequences of ECB signalling in tripartite synapses on the astrocyte-mediated regulation of synaptic function, which reveal novel properties of synaptic regulation by ECBs, such as the spatially controlled dual effect on synaptic strength and the lateral potentiation of synaptic efficacy. Finally, we discuss the potential implications of ECB signalling for astrocytes in brain pathology and animal behaviour.

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“…(Opposite.) (a) Under basal conditions, endocannabinoids modulate spinal nociceptive transmission through activation of pre- [10,24] and post-synaptic [25] CB1 receptors expressed on primary afferent fibres. Increased intracellular calcium ([ Ca 2þ ] i ) in postsynaptic neurons can stimulate AEA and 2-AG production and consequently activation of CB1 receptors.…”

Section: A Novel Role Of Cb2 Receptors In Chronic Pain Statesmentioning

confidence: 99%

Dynamic changes to the endocannabinoid system in models of chronic pain

Sagar

Burston

Woodhams

et al. 2012

Phil. Trans. R. Soc. B

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The analgesic effects of cannabinoid ligands, mediated by CB1 receptors are well established. However, the side-effect profile of CB1 receptor ligands has necessitated the search for alternative cannabinoid-based approaches to analgesia. Herein, we review the current literature describing the impact of chronic pain states on the key components of the endocannabinoid receptor system, in terms of regionally restricted changes in receptor expression and levels of key metabolic enzymes that influence the local levels of the endocannabinoids. The evidence that spinal CB2 receptors have a novel role in the modulation of nociceptive processing in models of neuropathic pain, as well as in models of cancer pain and arthritis is discussed. Recent advances in our understanding of the spinal location of the key enzymes that regulate the levels of the endocannabinoid 2-AG are discussed alongside the outcomes of recent studies of the effects of inhibiting the catabolism of 2-AG in models of pain. The complexities of the enzymes capable of metabolizing both anandamide (AEA) and 2-AG have become increasingly apparent. More recently, it has come to light that some of the metabolites of AEA and 2-AG generated by cyclooxygenase-2, lipoxygenases and cytochrome P450 are biologically active and can either exacerbate or inhibit nociceptive signalling.

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Neuronal and astrocytic localization of the cannabinoid receptor-1 in the dorsal horn of the rat spinal cord

Cited by 79 publications

References 20 publications

Cannabinoids and neuroinflammation

Cannabinoids and neuroinflammation

Astrocytes in endocannabinoid signalling

Dynamic changes to the endocannabinoid system in models of chronic pain

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