Levonantradol for Chemotherapy‐Induced Emesis: Phase I—II Oral Administration

László, John; Lucas, Virgil S.; Hanson, Dean; Cronin, Claire; Sallan, Stephen E.

doi:10.1002/j.1552-4604.1981.tb02573.x

Cited by 39 publications

(12 citation statements)

References 9 publications

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“…Altogether, these studies have M a n u s c r i p t 10 revealed a dose-dependent switch from reward to aversion, with low and high doses of cannabinoids inducing reward and aversion, respectively. An analogous phenomenon has been observed in human addicts, where low doses of THC or levonantradol are perceived as rewarding while higher doses as aversive (Noyes et al, 1975, Raft et al, 1977Laszlo et al, 1981).…”

supporting

confidence: 58%

Neurobiological mechanisms of cannabinoid addiction

Fattore

Fadda

Spano

et al. 2008

Molecular and Cellular Endocrinology

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Please cite this article as: Fattore, L., Fadda, P., Spano, M.S., Pistis, M., Fratta, W., Neurobiological mechanisms of cannabinoid addiction, Molecular and Cellular Endocrinology (2007), doi:10.1016/j.mce.2008 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. A c c e p t e d M a n u s c r i p t 2 AbstractThe endocannabinoid system is implicated in the regulation of a variety of physiological processes, among which conditioning, motivation, habit forming, memory, learning, and cognition play pivotal roles in drug reinforcement and reward. In this article we will give a synopsis of last developments in research on cannabinoid actions on brain reward circuits coming from behavioral, neurochemical and electrophysiological studies. Central cannabinoid-induced effects as measured by animal models of addiction, in vivo cerebral microdialysis, in vitro and in vivo electrophysiological recording techniques, will be reviewed.Brain sites that have been implicated in the mediation of addictive cannabinoid properties include primarily the ventral tegmental area, the nucleus accumbens, and the medial prefrontal cortex, although the amygdala, the substantia nigra, the globus pallidus, and the hippocampus have also been shown to be critical structures mediating motivational and reinforcing effects of cannabinoids. Putative neurobiological mechanisms underlying these effects will be delineated.

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supporting

confidence: 58%

Neurobiological mechanisms of cannabinoid addiction

Fattore

Fadda

Spano

et al. 2008

Molecular and Cellular Endocrinology

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“…It is well known that, with high doses, ∆ 9 -THC can cause dysphoria and even panic in human subjects (Raft et al 1977;Laszlo et al 1981). In laboratory animals, cannabinoids also possess an anxiogenic profile and stimulate the hypothalamo-pituitary axis in a manner similar to foot shock with a concomitant c-fos expression in stress-related loci (central and basolateral nuclei of the amygdala and periaqueductal grey in particular; Herkenham and Brady 1994).…”

Section: Discussionmentioning

confidence: 97%

Cannabinoid receptors and reward in the rat: a conditioned place preference study

2000

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“…This clinical application was thwarted as a result of the untoward side effects of memory impairment, cognitive dysfunction, and sedation [4,5], but has recently been reconsidered [6]. Although pharmaceutical development included treatment of nausea in cancer chemotherapy [7], the only CB 1 agonists to succeed to market have been dronabinol (also known as • 9 -tetrahydrocannabinol (THC)) and nabilone [8–10]. …”

Section: Cb1 Cannabinoid Receptor Physiology Pathology and Pharmacologymentioning

confidence: 99%

CB1 Cannabinoid Receptors and their Associated Proteins

Howlett¹,

Blume²,

Dalton³

2010

CMC

242

177

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CB1 receptors are G-protein coupled receptors (GPCRs) abundant in neurons, in which they modulate neurotransmission. The CB1 receptor influence on memory and learning is well recognized, and disease states associated with CB1 receptors are observed in addiction disorders, motor dysfunction, schizophrenia, and in bipolar, depression, and anxiety disorders. Beyond the brain, CB1 receptors also function in liver and adipose tissues, vascular as well as cardiac tissue, reproductive tissues and bone. Signal transduction by CB1 receptors occurs through interaction with Gi/o proteins to inhibit adenylyl cyclase, activate mitogen-activated protein kinases (MAPK), inhibit voltage-gated Ca2+ channels, activate K+ currents (Kir), and influence Nitric Oxide (NO) signaling. CB1 receptors are observed in internal organelles as well as plasma membrane. β-Arrestins, adaptor protein AP-3, and G-protein receptor-associated sorting protein 1 (GASP1) modulate cellular trafficking. Cannabinoid Receptor Interacting Protein 1a (CRIP1a) is an accessory protein whose function has not been delineated. Factor Associated with Neutral sphingomyelinase (FAN) regulates ceramide signaling. Such diversity in cellular signaling and modulation by interacting proteins suggests that agonists and allosteric modulators could be developed to specifically regulate unique, cell type-specific responses.

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Levonantradol for Chemotherapy‐Induced Emesis: Phase I—II Oral Administration

Cited by 39 publications

References 9 publications

Neurobiological mechanisms of cannabinoid addiction

Neurobiological mechanisms of cannabinoid addiction

Cannabinoid receptors and reward in the rat: a conditioned place preference study

CB1 Cannabinoid Receptors and their Associated Proteins

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