Opioid and cannabinoid receptor-mediated regulation of the increase in adrenocorticotropin hormone and corticosterone plasma concentrations induced by central administration of Δ9-tetrahydrocannabinol in rats

Manzanares, Jorge; Corchero, Javier; Fuentes, José A.

doi:10.1016/s0006-8993(99)01756-4

Cited by 150 publications

(92 citation statements)

References 24 publications

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“…Rimonabant, an antiobesity drug, increases CRH levels 84 while decreasing ACTH and cortisol at low doses, but increases both at high doses. 85 Traditional antidepressants such as fluoxetine, citalopram and imipramine all decrease CRH, ACTH and cortisol levels. [86][87][88][89] A slight rise in CRH may be detected immediately after starting treatment with citalopram, which turns into a decrease after continuous administration.…”

Section: A B C D E F G Hmentioning

confidence: 99%

Approaching the shared biology of obesity and depression: the stress axis as the locus of gene–environment interactions

et al. 2006

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Obesity and depression are serious public health problems and also constitute cardiovascular disease risk factors. Research organizations have called for efforts to explore the interrelationship between obesity and depression. A useful starting point is the fact that in both disorders there is dysregulation of stress systems. We review molecular and clinical evidence indicating that the mediators of the stress response are a key locus for geneenvironment interactions in the shared biology of depression and obesity. Scientific milestones include translational paradigms such as mice knockouts, imaging and pharmacogenomic approaches that can identify new therapeutic strategies for those burdened by these two afflictions of contemporary civilization. Perspectives for the future are promising. Our ability to dissect the underpinnings of common and complex diseases with shared substrates will be greatly enhanced by the Genes and Environment Initiative, the emerging Large Scale Studies of Genes and Environment in Common Disease, and the UK Biobank Project.

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Section: A B C D E F G Hmentioning

confidence: 99%

Approaching the shared biology of obesity and depression: the stress axis as the locus of gene–environment interactions

et al. 2006

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“…However, recent evidence suggests that some or even most of the GPCR are oligomeric structures formed by GPCR homodimers, heterodimers, multimers, and also different types of proteins that intercommunicate at the plasma membranes (1 -3). It is well known that opioids that bind to G protein-coupled μ-opioid receptors (μOR) and cannabinoids that bind to G protein-coupled cannabinoid receptors (CB 1 R) expressed in the central nervous system have common pharmacological effects, such as antinociception, hypothermia, inhibition of locomotor activity, hypotension, and sedation (4,5). The synergy in the analgesic effects of opioids and cannabinoids is attributed to a cross-talk between these two signaling pathways mediated by simultaneous activation of opioid and cannabinoid receptors.…”

Section: Introductionmentioning

confidence: 99%

μ-Opioid Receptor Forms a Functional Heterodimer With Cannabinoid CB1 Receptor: Electrophysiological and FRET Assay Analysis

et al. 2008

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Abstract. Interactions between μ-opioid receptor (μOR) and cannabinoid CB 1 receptor (CB 1 R) were examined by morphological and electrophysiological methods. In baby hamster kidney (BHK) cells coexpressing μOR fused to the yellow fluorescent protein Venus and CB 1 R fused to the cyan fluorescent protein Cerulean, both colors were detected on the cell surface; and fluorescence resonance energy transfer (FRET) analysis revealed that μOR and CB 1 R formed a heterodimer. Coimmunoprecipitation and Western blotting analyses also confirmed the heterodimers of μOR and CB 1 R. [D-Ala 2 ,N-Me-Phe 4 ,Gly 5 -ol]enkephalin (DAMGO) or CP55,940 elicited K + currents in Xenopus oocytes expressing μOR or CB 1 R together with G protein activated-inwardly rectifying K + channels (GIRKs), respectively. In oocytes coexpressing both receptors, either of which was fused to the chimeric Gα protein G qi5 that activates the phospholipase C pathway, both DAMGO and CP55,940 elicited Ca 2+ -activated Cl − currents, indicating that each agonist can induce responses through G qi5 fused to either its own receptor or the other. Experiments with endogenous G i/o protein inactivation by pertussis toxin (PTX) supported the functional heterodimerization of μOR/ CB 1 R through PTX-insensitive G qi5(m) fused to each receptor. Thus, μOR and CB 1 R form a heterodimer and transmit a signal through a common G protein. Our electrophysiological method could be useful for determination of signals mediated through heterodimerized G protein-coupled receptors.

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“…However, evidence is accumulating that tonic activation of CB 1 receptors exerts a stressinhibitory effect. For example, blockade of endogenous CB 1 receptor activity with rimonabant increases adrenocorticotropin hormone and corticosterone plasma concentrations (Manzanares et al, 1999). Similarly, basal adrenocorticotropin hormone concentrations are increased in CB 1 receptor null mice (Haller et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Interactions between endocannabinoids and stress-induced decreased sensitivity to natural reward

Rademacher

Hillard

2007

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Since endocannabinoids modulate reward processing and the stress response, we tested the hypothesis that endocannabinoids regulate stress-induced decreased sensitivity to natural reward. Restraint was used to produce stress-induced reductions in sucrose consumption and preference in male mice. Central cannabinoid receptor (CB 1 ) signaling was modulated pharmacologically prior to the application of stress. The preference for sucrose over water was significantly decreased in mice exposed to restraint. Treatment of mice with a cannabinoid receptor agonist (CP55940) or fatty acid amide hydrolase inhibitor (URB597) attenuated, while the CB 1 receptor antagonist/inverse agonist, rimonabant (SR141716), enhanced, stress-induced decreases in sucrose preference. These data are consistent with a tonically active, stress-inhibitory role for the CB 1 receptor. Mice treated with 10 daily episodes of restraint showed reduced sucrose preference that was unaffected by CP55940 and URB597. However, rimonabant produced a greater reduction in sucrose preference on day 10 compared to day 1. These data suggest that on day 10, endocannabinoid signaling is maximally activated and essential for reward sensitivity. The findings of the present study indicate that the CB 1 /endocannabinoid signaling system is an important allostatic mediator that both modulates the responses of mice to stress and is itself modulated by stress.

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Opioid and cannabinoid receptor-mediated regulation of the increase in adrenocorticotropin hormone and corticosterone plasma concentrations induced by central administration of Δ9-tetrahydrocannabinol in rats

Cited by 150 publications

References 24 publications

Approaching the shared biology of obesity and depression: the stress axis as the locus of gene–environment interactions

Approaching the shared biology of obesity and depression: the stress axis as the locus of gene–environment interactions

μ-Opioid Receptor Forms a Functional Heterodimer With Cannabinoid CB1 Receptor: Electrophysiological and FRET Assay Analysis

Interactions between endocannabinoids and stress-induced decreased sensitivity to natural reward

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