Endogenous fatty acid ethanolamides suppress nicotine-induced activation of mesolimbic dopamine neurons through nuclear receptors
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PPAR-alpha agonists as novel antiepileptic drugs: preclinical findingsHub and switches: endocannabinoid signalling in midbrain dopamine neuronsA fatty gut feelingInhibition of FAAH and activation of PPAR: new approaches to the treatment of cognitive dysfunction and drug addictionFatty acid amide hydrolase as a potential therapeutic target for the treatment of pain and CNS disordersInternational Union of Basic and Clinical Pharmacology. LXXIX. Cannabinoid receptors and their ligands: beyond CB₁ and CB₂Neuroprotective activities of palmitoylethanolamide in an animal model of Parkinson's diseaseBlockade of nicotine reward and reinstatement by activation of alpha-type peroxisome proliferator-activated receptorsMaternal Immune Activation Disrupts Dopamine System in the OffspringEffects of drugs of abuse on putative rostromedial tegmental neurons, inhibitory afferents to midbrain dopamine cellsDual blockade of FAAH and MAGL identifies behavioral processes regulated by endocannabinoid crosstalk in vivo.In vivo pharmacology of endocannabinoids and their metabolic inhibitors: therapeutic implications in Parkinson's disease and abuse liabilityAM404 attenuates reinstatement of nicotine seeking induced by nicotine-associated cues and nicotine priming but does not affect nicotine- and food-taking.Peroxisome proliferator-activated receptors-alpha modulate dopamine cell activity through nicotinic receptors.The endocannabinoid system as a target for the treatment of neurodegenerative disease.Animal models of cannabinoid reward.Palmitoylethanolamide protects against the amyloid-β25-35-induced learning and memory impairment in mice, an experimental model of Alzheimer disease.The role of fatty acid amide hydrolase inhibition in nicotine reward and dependence.Anti-kindling Effect of Bezafibrate, a Peroxisome Proliferator-activated Receptors Alpha Agonist, in Pentylenetetrazole Induced Kindling Seizure Model.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.Endocannabinoid influence in drug reinforcement, dependence and addiction-related behaviors.Dietary triacylglycerols with palmitic acid in the sn-2 position modulate levels of N-acylethanolamides in rat tissuesNovel use of a lipid-lowering fibrate medication to prevent nicotine reward and relapse: preclinical findings.New insights on endocannabinoid transmission in psychomotor disorders.The anandamide transport inhibitor AM404 reduces the rewarding effects of nicotine and nicotine-induced dopamine elevations in the nucleus accumbens shell in rats.Effects of Fatty Acid Amide Hydrolase (FAAH) Inhibitors in Non-Human Primate Models of Nicotine Reward and RelapsePlasma Endocannabinoid Alterations in Individuals with Substance Use Disorder are Dependent on the "Mirror Effect" of SchizophreniaRole of the satiety factor oleoylethanolamide in alcoholism.The FAAH inhibitor URB597 efficiently reduces tyrosine hydroxylase expression through CB₁- and FAAH-independent mechanisms.Putative Epigenetic Involvement of the Endocannabinoid System in Anxiety- and Depression-Related Behaviors Caused by Nicotine as a StressorPeroxisome proliferator-activated receptor (PPAR) agonists as promising new medications for drug addiction: preclinical evidence.Sex-specific tonic 2-arachidonoylglycerol signaling at inhibitory inputs onto dopamine neurons of Lister Hooded ratsMutation of putative GRK phosphorylation sites in the cannabinoid receptor 1 (CB1R) confers resistance to cannabinoid tolerance and hypersensitivity to cannabinoids in miceOleoylethanolamide: a novel potential pharmacological alternative to cannabinoid antagonists for the control of appetiteThe genetic basis of the endocannabinoid system and drug addiction in humans.Anandamide and 2-arachidonoylglycerol: pharmacological properties, functional features, and emerging specificities of the two major endocannabinoids.Using dopamine research to generate rational cannabinoid drug policy.Interplay between synaptic endocannabinoid signaling and metaplasticity in neuronal circuit function and dysfunction.Fatty acid amide hydrolase (FAAH) inactivation confers enhanced sensitivity to nicotine-induced dopamine release in the mouse nucleus accumbens.Interactions between the endocannabinoid and nicotinic cholinergic systems: preclinical evidence and therapeutic perspectives.
P2860
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P2860
Endogenous fatty acid ethanolamides suppress nicotine-induced activation of mesolimbic dopamine neurons through nuclear receptors
description
2008 nî lūn-bûn
@nan
2008 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2008 թվականի դեկտեմբերին հրատարակված գիտական հոդված
@hy
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
@yue
name
Endogenous fatty acid ethanola ...... rons through nuclear receptors
@ast
Endogenous fatty acid ethanola ...... rons through nuclear receptors
@en
type
label
Endogenous fatty acid ethanola ...... rons through nuclear receptors
@ast
Endogenous fatty acid ethanola ...... rons through nuclear receptors
@en
prefLabel
Endogenous fatty acid ethanola ...... rons through nuclear receptors
@ast
Endogenous fatty acid ethanola ...... rons through nuclear receptors
@en
P2093
P2860
P1476
Endogenous fatty acid ethanola ...... rons through nuclear receptors
@en
P2093
Anna Lisa Muntoni
Marco Pistis
Miriam Melis
Sevil Yasar
Steven R Goldberg
P2860
P304
13985-13994
P356
10.1523/JNEUROSCI.3221-08.2008
P407
P577
2008-12-01T00:00:00Z