This page lists works of an author who doesn't have a ResearchGate profile or hasn't added the works to their profile yet. It is automatically generated from public (personal) data to further our legitimate goal of comprehensive and accurate scientific recordkeeping. If you are this author and want this page removed, please let us know.
December 2010
·
19 Reads
ChemInform
ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.
November 2010
·
60 Reads
·
105 Citations
Current Medicinal Chemistry
In agreement with the highly lipophilic nature of (-)-delta9-tetrahydrocannabinol, all the endogenous ligands of cannabinoid receptors identified so far are derivatives of long chain fatty acids. N- Arachidonoylethanolamine (anandamide) and some of its polyunsaturated congeners have been found in mammalian brain and shown to activate the CB1 and, with a lower efficacy, CB2 cannabinoid receptor subtypes. More recently, 2-arachidonoylglycerol (2-AG), a widespread intermediate in the metabolism of phosphoglycerides, diacylglycerols and triglycerides, was also found to activate the cannabinoid receptors. The capability of palmitoylethanolamide, an anti-inflammatory metabolite, to activate CB2-like receptors is still being debated. Here we review: 1) the metabolic pathways suggested so far to underlie the biosynthesis and inactivation of anandamide and 2-AG, and 2) the current knowledge of the chemical bases for the interactions of anandamide and 2-AG with proteins of the endogenous cannabinoid system characterized so far, i.e. the CB1 and CB2 receptor subtypes, the membrane anandamide carrier , which facilitates anandamide diffusion into cells, and the enzyme fatty acid amide hydrolase , which catalyzes anandamide and, to a certain extent, 2-AG hydrolysis in vivo.
July 2010
·
19 Reads
ChemInform
ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.
May 2010
·
13 Reads
ChemInform
ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.
March 2010
·
10 Reads
·
23 Citations
ChemInform
ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.
March 2010
·
9 Reads
·
5 Citations
ChemInform
ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.
February 2010
·
26 Reads
·
6 Citations
ChemInform
The four diastereomers of 1′,2′-dimethylheptyl-Δ8-THC (2) have been synthesized. Pharmacology both in vitro and in vivo indicated that all four isomers were very potent cannabinoids. The 1′R,2′S and 1′S,2′R are considerably more potent than the other two isomers, and are among the most potent traditional cannabinoids known.
February 2010
·
11 Reads
ChemInform
ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.
March 2009
·
17 Reads
·
31 Citations
Neuropharmacology
Affective nicotine withdrawal symptoms are of major motivational significance in contributing to relapse and continued tobacco use; thus, it is important to understand the molecular and receptor-mediated mechanisms that mediate affective withdrawal behaviors. Previous work using the conditioned place aversion (CPA) model has shown that nicotine withdrawal is associated with a negative affective state, and place aversion to previously neutral environmental stimuli represents a motivational component in the maintenance of drug use. Thus, the purpose of this study was to evaluate the role of genotype, sex, and age and to extend previous studies examining the role of various nicotinic receptor subtypes in the development of nicotine withdrawal aversion using the CPA model. Mice were chronically treated with nicotine and conditioned for two days with various nicotinic receptor antagonists. The major findings showed that mecamylamine and dihydro-beta-erythroidine (DHbetaE), but not hexamethonium or methyllycaconitine citrate (MLA), precipitated significant aversion in the CPA model. This pharmacological data support our previous knockout mouse data suggesting that nicotine CPA is mediated by central beta2-containing nicotinic receptors, but not alpha7 nicotinic receptors. Further, we show that sex and age are contributing factors to the development of nicotine CPA. Overall, the results of our study provide some insight into pharmacological and behavioral factors involved in the development of an aversive motivational component associated with nicotine withdrawal.
September 2008
·
22 Reads
·
115 Citations
Journal of Pharmacology and Experimental Therapeutics
A growing body of evidence suggests that the endogenous cannabinoid system modulates the addictive properties of nicotine, the main component of tobacco that produces rewarding effects. In our study, complementary transgenic and pharmacological approaches were used to test the hypothesis that the endocannabinoid system modulates nicotine reward and dependence. An acute injection of nicotine elicited normal analgesic and hypothermic effects in cannabinoid receptor (CB)(1) knockout (KO) mice and mice treated with the CB(1) antagonist rimonabant. However, disruption of CB(1) receptor signaling blocked nicotine reward, as assessed in the conditioned place preference (CPP) paradigm. In contrast, genetic deletion, or pharmacological inhibition of fatty acid amide hydrolase (FAAH), the enzyme responsible for catabolism of the endocannabinoid anandamide, enhanced the expression of nicotine CPP. Although the expression of spontaneous nicotine withdrawal (14 days, 24 mg/kg/day nicotine) was unaffected in CB(1) KO mice, acute administration of rimonabant (3 mg/kg) ameliorated somatic withdrawal signs in wild-type mice. Increasing endogenous levels of anandamide through genetic or pharmacological approaches exacerbated the physical somatic signs of spontaneous nicotine withdrawal in a milder withdrawal model (7 days, 24 mg/kg/day nicotine). Moreover, FAAH-compromised mice displayed increased conditioned place aversion in a mecamylamine-precipitated model of nicotine withdrawal. These findings indicate that endocannabinoids play a role in the rewarding properties of nicotine as well as nicotine dependence liability. Specifically, increasing endogenous cannabinoid levels magnifies, although disrupting CB(1) receptor signaling, attenuates nicotine reward and withdrawal. Taken together, these results support the hypothesis that cannabinoid receptor antagonists may offer therapeutic advantages to treat tobacco dependence.
... It was first identified in the cerebrospinal fluid of sleep-deprived cats (Cravatt et al., 1995). Because of their similar structures, oleamide and anandamide evoke similar effects (Divito and Cascio, 2013) including sleep induction (Herrera-Solis et al., 2010), hypothermia, hypomotility, and analgesia (Smith et al., 1994;Fedorova et al., 2001). Oleamide is an agonist of CB1 receptors (Leggett et al., 2004). ...
July 1994
Journal of Pharmacology and Experimental Therapeutics
... Disruption in lipid homeostasis may lead to cholinergic dysfunction, due changes in phospholipid and sphingolipid pathways that are critical for cell membrane repair and production of the neurotransmitter acetylcholine (ACh), which are affected in AD [25,26]. Since cannabinoid 1 (CB 1 ) and sphingosine 1-phosphate 1 (S1P 1 ) receptors are the most widespread lipidic neuromodulators within the central nervous system and their endogenous ligands are derived from membrane lipid precursors, changes in the activity of these receptors likely play a key role in the modification of lipid homeostasis [27][28][29], which may be altered in AD. In this regard, CB 1 activity is increased following basal forebrain cholinergic denervation [30] and the modulation of the release of ACh in rat cortex [31], suggesting an interaction between cannabinoid and cholinergic systems resulting from cannabinoid activation via muscarinic receptors [32,33]. ...
August 1999
Current Medicinal Chemistry
... The positive reinforcing effects of cannabinoids had been difficult to determine in non-human primates given that early studies failed to reliably demonstrate behaviour maintained by THC and synthetic cannabinoids (Carney, Uwaydah, & Balster, 1977;Harris, Waters, & McLendon, 1974;Leite & Carlini, 1974;Mansbach, Nicholson, Martin, & Balster, 1994;Pickens, Thompson, & Muchow, 1973). Only recently has reliable dose-dependent self-administration of intravenous THC been reported in cocaine-experienced (Tanda, Munzar, & Goldberg, 2000) and drug-naïve monkeys (Justinova, Tanda, Redhi, & Goldberg, 2003). ...
January 1994
Behavioural Pharmacology
... A defining feature of drug dependence resulting from chronic exposure to other classes of drugs, for example, opioids or benzodiazepines (e.g., Gellert and Holtzman, 1979;Lukas and Griffiths, 1982) is the ability of receptor antagonists to precipitate overt, pronounced signs of withdrawal, and previous studies have shown that the stimulus properties of 24 h abstinence after chronic treatment with 9 -THC or AM2389 overlap with those of rimonabant in non-human primates (Stewart and McMahon, 2010;Kangas et al., 2020). Studies in rodents and non-human primates that are chronically treated with 9 -THC or other CB 1 agonists have further suggested that rimonabant-precipitated withdrawal can be characterized by overt signs including paw tremor and head shakes (Verberne et al., 1981;Cook et al., 1998;Stewart and McMahon, 2010). However, this remains controversial, as such behavioral disturbances can be produced by rimonabant alone (including psychiatric side effects that led to its withdrawal from market; Nguyen et al., 2019) and are not always apparent in subjects treated with cannabinoids like 9 -THC or AM2389 (Kangas et al., 2020). ...
June 1998
Journal of Pharmacology and Experimental Therapeutics
... However, when given at low doses in combination with another drug, they can have the same therapeutic effect, but with fewer side effects. Cannabinoids and opioids both produce analgesia and are of particular interest in the context of clinical pain management (Gennings et al., 1994). An example of an opioid is morphine and an example of cannabinoids is 9 -tetrahydro-cannabinol ( 9 -THC), which is the active ingredient in marijuana. ...
January 1994
... Cannabinoids elicit a marked extrapyramidal motor disturbance in animals, catalepsy (Compton et al., 1996; Sanudo-Pena et al., 1999). SNR neurons are the main output neurons of the basal ganglia, and enhancement of their ¢ring rate is thought to lead to catalepsy (Havemann et al., 1983; Kolasiewicz et al., 1988). ...
January 1996
Handbook of Experimental Pharmacology
... We found that carbachol, given i.c.v. to conscious rats, elicited a dose dependent, significant increase in ACTH and corticosterone secretion which was totally abolished by i.c.v. pretreatment with cholinergic antagonist atropine but was not affected by pretreatment with a selective nicotinic receptor antagonist mecamylamine (10,16). This finding corroborates the concept that cholinergic neurons modulate the HPA axis predominantly via stimulation of hypothalamic release of CRH and central muscarinic receptors play a significant role in this stimulation. ...
January 1996
Medicinal Chemistry Research
... Structures of IPH, [ 125 I]IPH and EB. were corrected for the amount of ligand bound to tissue, which was consistently 20% of the total ligand present. Romano and Goldstein, 1980; Schwartz et al., 1982; Marks and Collins, 1982;) but not between those of EB (Badio and Daly, 1994; Damaj et al., 1994; Dukat et al., 1993; Houghtling et al., 1995). The ()-and ()-isomers of EB also appear to be equipotent in activating nicotinic receptors (Badio and Daly, 1994; Damaj et al., 1994; Li et al., 1993). ...
March 2010
ChemInform
... CB1R is a protein that is encoded by the CNR1 gene and has 472 amino acids in humans and 473 amino acids in rats and mice, with 97-99% amino acid sequence similarity [19]. been linked to cannabis addiction in several studies [20,21]. Structures of some cannabinoid receptor agonists and antagonists are mentioned below in Fig. (1). ...
January 2002
Chemistry and Physics of Lipids
... Il est clairement établi que l'activation centrale du SEC stimule la prise alimentaire et que l'augmentation du taux des deux principaux endocannabinoïdes agonistes des CB1R, l'AEA et le 2-AG, est associée à la prise de poids (Di Marzo et al., 2001a;Jamshidi and Taylor, 2001;Williams and Kirkham, 1999). Figure 11 : Conséquences de l'activation du CB1R sur les organes impliqués dans la régulation de l'homéostasie énergétique (Deveaux, 2008 ...
January 2001
Biochemical and Biophysical Research Communications
