Effects of fatty acid amide hydrolase inhibition on neuronal responses to nicotine, cocaine and morphine in the nucleus accumbens shell and ventral tegmental area: involvement of PPAR-alpha nuclear receptors.

Effects of fatty acid amide hydrolase inhibition on neuronal responses to nicotine, cocaine and morphine in the nucleus accumbens shell and ventral tegmental area: involvement of PPAR-alpha nuclear receptors.

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http://www.wikidata.org/entity/Q35196626

Q35196626

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Hub and switches: endocannabinoid signalling in midbrain dopamine neurons Modulation of the endocannabinoid system: vulnerability factor and new treatment target for stimulant addiction Inhibition of FAAH and activation of PPAR: new approaches to the treatment of cognitive dysfunction and drug addiction Endocannabinoid signalling in reward and addiction.The cannabinoid CB2 receptor is necessary for nicotine-conditioned place preference, but not other behavioral effects of nicotine in mice The role of fatty acid amide hydrolase inhibition in nicotine reward and dependence.Role of the endogenous cannabinoid system in nicotine addiction: novel insights.Endocannabinoid influence in drug reinforcement, dependence and addiction-related behaviors.Novel use of a lipid-lowering fibrate medication to prevent nicotine reward and relapse: preclinical findings.Effects of Fatty Acid Amide Hydrolase (FAAH) Inhibitors in Non-Human Primate Models of Nicotine Reward and Relapse Ventral tegmental area dopamine and GABA neurons: Physiological properties and expression of mRNA for endocannabinoid biosynthetic elements.Role of the satiety factor oleoylethanolamide in alcoholism.The FAAH inhibitor URB597 efficiently reduces tyrosine hydroxylase expression through CB₁- and FAAH-independent mechanisms.Cocaine-induced endocannabinoid release modulates behavioral and neurochemical sensitization in mice Anandamide and 2-arachidonoylglycerol: pharmacological properties, functional features, and emerging specificities of the two major endocannabinoids.Fatty acid amide hydrolase (FAAH) inactivation confers enhanced sensitivity to nicotine-induced dopamine release in the mouse nucleus accumbens.An Introduction to the Endogenous Cannabinoid System.Interactions between the endocannabinoid and nicotinic cholinergic systems: preclinical evidence and therapeutic perspectives.An update on PPAR activation by cannabinoids.Cannabinoid Modulation of Memory Consolidation in Rats: Beyond the Role of Cannabinoid Receptor Subtype 1 Inhibition of FAAH confers increased stem cell migration via PPARα Inhibitory inputs from rostromedial tegmental neurons regulate spontaneous activity of midbrain dopamine cells and their responses to drugs of abuse Nicotine reinforcement is reduced by cannabinoid CB1 receptor blockade in the ventral tegmental area.Oleoylethanolamide dose-dependently attenuates cocaine-induced behaviours through a PPARα receptor-independent mechanism.Oleoylethanolamide-induced anorexia in rats is associated with locomotor impairment.Attenuation of cue-induced reinstatement of nicotine seeking by URB597 through cannabinoid CB1 receptor in rats.The peroxisome proliferator-activated receptor alpha agonist fenofibrate attenuates alcohol self-administration in rats.

P2860

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P2860

Effects of fatty acid amide hydrolase inhibition on neuronal responses to nicotine, cocaine and morphine in the nucleus accumbens shell and ventral tegmental area: involvement of PPAR-alpha nuclear receptors.

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http://www.wikidata.org/entity/Q35196626

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2010 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2010年の論文

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