The effects of Δ1-tetrahydrocannabinol on cyclic AMP levels in WI-38 fibroblasts

Kelly, Lewis; Butcher, R.W.

doi:10.1016/0304-4165(73)90335-8

Cited by 19 publications

(5 citation statements)

References 6 publications

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“…Previously, D 9 -THC at low concentrations was shown to increase cyclic AMP levels and cyclic AMP-dependent protein kinase activity in human cultured lung cells (Kelly & Butcher, 1979) and basal adenylyl cyclase activity in mouse cerebral cortical homogenates (Hillard & Bloom, 1983). We have shown similar e ects with the synthetic cannabinoid WIN 55,212-2 in the globus pallidus and been able to demonstrate the involvement of a receptor-mediated action by virtue of blockade by the selective cannabinoid receptor antagonist SR 141716A.…”

supporting

confidence: 59%

Paradoxical action of the cannabinoid WIN 55,212‐2 in stimulated and basal cyclic AMP accumulation in rat globus pallidus slices

Maneuf

Brotchie

1997

British J Pharmacology

104

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The e ects of the synthetic cannabinoid WIN 55,212-2 on forskolin-stimulated and basal adenosine 3' : 5'-cyclic monophosphate (cyclic AMP) accumulation in globus pallidus slices were investigated. WIN 55,212-2 caused a concentration-dependent decrease in forskolin-stimulated cyclic AMP accumulation in globus pallidus slices (maximum inhibition 36% for 30 mM). This e ect was blocked by the cannabinoid receptor antagonist SR 141716A (100 mM). WIN 55,212-2 alone caused a concentration-dependent increase in cyclic AMP levels in unstimulated slices (maximum increase 52.6% for 100 mM). This e ect was also blocked by SR 141716A (100 mM). In either forskolin-stimulated or unstimulated conditions SR 1417161A (100 mM) did not a ect cyclic AMP levels.

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supporting

confidence: 59%

Paradoxical action of the cannabinoid WIN 55,212‐2 in stimulated and basal cyclic AMP accumulation in rat globus pallidus slices

Maneuf

Brotchie

1997

British J Pharmacology

104

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“…55 In earlier studies, THC-induced bronchodilation was found not to be me diated by stimulation of beta-adrenergic receptors or blockade of muscarinic receptors on airway smooth muscle. 56,57 However, that THC might still have a parasympatholytic effect at a cholinergic site proximal to the muscarinic receptor on airway smooth muscle was suggested by evidence that it inhibited the release of acetylcholine from postganglionic nerve endings fol lowing vagal and chorda tympani stimulation in dogs 58 and the myenteric plexus in guinea pigs. 59 THC is now known to act through specific seven-transmembrane inhibitory G-protein-coupled cannabinoid receptors:…”

Section: Short-term Physiological Effectsmentioning

confidence: 99%

Respiratory and Immunologic Consequences of Marijuana Smoking

Tashkin

Baldwin

Sarafian

et al. 2002

The Journal of Clinical Pharma

157

122

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Habitual smoking of marijuana has a number of effects on the respiratory and immune systems that may be clinically relevant. These include alterations in lung function ranging from no to mild airflow obstruction without evidence of diffusion impairment, an increased prevalence of acute and chronic bronchitis, striking endoscopic findings of airway injury (erythema, edema, and increased secretions) that correlate with histopathological alterations in bronchial biopsies, and dysregulated growth of the bronchial epithelium associated with altered expression of nuclear and cytoplasmic proteins involved in the pathogenesis of bronchogenic carcinoma. Other consequences of regular marijuana use include ultrastructual abnormalities in human alveolar macrophages along with impairment of their cytokine production, antimicrobial activity, and tumoricidal function. Cannabinoid receptor expression is altered in leukocytes collected from the blood of chronic smokers, and experimental models support a role for delta9-tetrahydrocannabinol in suppressing T cell function and cell-mediated immunity. The potential for marijuana smoking to predispose to the development of respiratory malignancy is suggested by several lines of evidence, including the presence of potent carcinogens in marijuana smoke and their resulting deposition in the lung, the occurrence of premalignant changes in bronchial biopsies obtained from smokers of marijuana in the absence of tobacco, impairment of antitumor immune defenses by delta9-tetrahydrocannabinol, and several clinical case series in which marijuana smokers were disproportionately over represented among young individuals who developed upper or lower respiratory tract cancer. Additional well designed epidemiological and immune monitoring studies are required to determine the potential causal relationship between marijuana use and the development of respiratory infection and/or cancer.

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“…However, the CB 1 receptor‐mediated facilitatory effect of Δ 9 ‐THC on extracellular glutamate levels is consistent with other studies indicating the existence of excitatory actions of CB 1 receptor agonists, especially under resting conditions. In particular, it has been shown that at low concentrations Δ 9 ‐THC increased cAMP accumulation and cAMP‐dependent protein kinase activity in human cultured lung cells (Kelly and Butcher, 1979). Furthermore, activation of CB 1 receptor‐mediated increase in basal adenyl cyclase activity and of protein kinase C has been found not only in the periphery but also in the CNS, especially in the cerebral cortex and forebrain (Hillard and Bloom, 1983; Hillard and Auchampach, 1994).…”

Section: Discussionmentioning

confidence: 99%

Δ⁹‐tetrahydrocannabinol increases endogenous extracellular glutamate levels in primary cultures of rat cerebral cortex neurons: Involvement of CB₁ receptors

Tomasini¹,

Ferraro²,

Bebe³

et al. 2002

J of Neuroscience Research

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The effects of the principal psychoactive component of marijuana, Delta(9)-tetrahydrocannabinol (Delta(9)-THC), on endogenous extracellular glutamate levels in primary cultures of rat cerebral cortex neurons were investigated. Locally applied Delta(9)-THC (0.03, 3, 300, and 1,000 nM) concentration-dependently increased basal extracellular glutamate levels (+18% +/- 11%, +54% +/- 10%, +90% +/- 14%, +149% +/- 33% vs. basal). The facilitatory effects of Delta(9)-THC (3 and 300 nM) on cortical glutamate were fully counteracted in the presence of the selective CB(1) receptor antagonist SR141716A (10 nM) and by replacement of the normal Krebs-Ringer bicarbonate buffer with a low-Ca(2+) (0.2 mM) medium. Delta(9)-THC application also induced an enhancement in K(+)-evoked glutamate levels. These findings suggest that an increase in cortical glutamatergic transmission mediated by local CB(1) receptor activation may underlie some of the psychoactive and behavioral effects of acute marijuana consumption.

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The effects of Δ1-tetrahydrocannabinol on cyclic AMP levels in WI-38 fibroblasts

Cited by 19 publications

References 6 publications

Paradoxical action of the cannabinoid WIN 55,212‐2 in stimulated and basal cyclic AMP accumulation in rat globus pallidus slices

Paradoxical action of the cannabinoid WIN 55,212‐2 in stimulated and basal cyclic AMP accumulation in rat globus pallidus slices

Respiratory and Immunologic Consequences of Marijuana Smoking

Δ⁹‐tetrahydrocannabinol increases endogenous extracellular glutamate levels in primary cultures of rat cerebral cortex neurons: Involvement of CB₁ receptors

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The effects of Δ1-tetrahydrocannabinol on cyclic AMP levels in WI-38 fibroblasts

Cited by 19 publications

References 6 publications

Paradoxical action of the cannabinoid WIN 55,212‐2 in stimulated and basal cyclic AMP accumulation in rat globus pallidus slices

Paradoxical action of the cannabinoid WIN 55,212‐2 in stimulated and basal cyclic AMP accumulation in rat globus pallidus slices

Respiratory and Immunologic Consequences of Marijuana Smoking

Δ9‐tetrahydrocannabinol increases endogenous extracellular glutamate levels in primary cultures of rat cerebral cortex neurons: Involvement of CB1 receptors

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Δ⁹‐tetrahydrocannabinol increases endogenous extracellular glutamate levels in primary cultures of rat cerebral cortex neurons: Involvement of CB₁ receptors