| Q55236616 | A Pharmacological Rationale to Reduce the Incidence of Opioid Induced Tolerance and Hyperalgesia: A Review. |
| Q30429221 | ACSL6 is associated with the number of cigarettes smoked and its expression is altered by chronic nicotine exposure |
| Q47225379 | Acute and chronic modulation of striatal endocannabinoid-mediated plasticity by nicotine |
| Q38026790 | Anandamide and 2-arachidonoylglycerol: pharmacological properties, functional features, and emerging specificities of the two major endocannabinoids. |
| Q34098204 | Animal models of cannabinoid reward |
| Q36900018 | Animal models of nicotine exposure: relevance to second-hand smoking, electronic cigarette use, and compulsive smoking. |
| Q90217765 | Behavioral effects of psychostimulants in mutant mice with cell-type specific deletion of CB2 cannabinoid receptors in dopamine neurons |
| Q90524726 | Brain activity of anandamide: a rewarding bliss? |
| Q37444808 | Cannabinoid CB1 receptor antagonists as potential pharmacotherapies for drug abuse disorders |
| Q41573121 | Cannabinoid Receptor 1 and Fatty Acid Amide Hydrolase Contribute to Operant Sensation Seeking in Mice |
| Q30365559 | Constitutional mechanisms of vulnerability and resilience to nicotine dependence |
| Q30470474 | Decreased reward sensitivity in rats from the Fischer344 strain compared to Wistar rats is paralleled by differences in endocannabinoid signaling |
| Q34973799 | Differential effects of endocannabinoid catabolic inhibitors on morphine withdrawal in mice |
| Q64984123 | Dose-Response Effect of Antibodies to S100 Protein and Cannabinoid Receptor Type 1 in Released-Active Form in the Light-Dark Test in Mice. |
| Q34575484 | Drug addiction. |
| Q30492114 | Dual blockade of FAAH and MAGL identifies behavioral processes regulated by endocannabinoid crosstalk in vivo. |
| Q36184904 | Effects of Fatty Acid Amide Hydrolase (FAAH) Inhibitors in Non-Human Primate Models of Nicotine Reward and Relapse |
| Q35196626 | 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. |
| Q28236453 | Emerging drugs for the treatment of tobacco dependence: 2014 update |
| Q35532072 | Endocannabinoid influence in drug reinforcement, dependence and addiction-related behaviors |
| Q27311588 | Endocannabinoid regulation of acute and protracted nicotine withdrawal: effect of FAAH inhibition |
| Q30373359 | Endocannabinoid signalling in reward and addiction. |
| Q29042501 | Endocannabinoid-mediated synaptic plasticity and addiction-related behavior |
| Q33583792 | Endocannabinoids and striatal function: implications for addiction-related behaviours |
| Q38665296 | Fatty acid amide hydrolase (FAAH) inactivation confers enhanced sensitivity to nicotine-induced dopamine release in the mouse nucleus accumbens |
| Q51943546 | Genetic Models of the Endocannabinoid System |
| Q26853457 | Genetic matters: thirty years of progress using mouse models in nicotinic research |
| Q33751118 | In vivo pharmacology of endocannabinoids and their metabolic inhibitors: therapeutic implications in Parkinson's disease and abuse liability |
| Q28283718 | Inhibition of FAAH and activation of PPAR: new approaches to the treatment of cognitive dysfunction and drug addiction |
| Q37146387 | Inhibition of anandamide hydrolysis by cyclohexyl carbamic acid 3'-carbamoyl-3-yl ester (URB597) reverses abuse-related behavioral and neurochemical effects of nicotine in rats |
| Q45988694 | Inhibition of fatty acid amide hydrolase reduces reinstatement of nicotine seeking but not break point for nicotine self-administration--comparison with CB(1) receptor blockade. |
| Q34994542 | Inhibition of monoacylglycerol lipase reduces nicotine withdrawal |
| Q38686274 | Interactions between the endocannabinoid and nicotinic cholinergic systems: preclinical evidence and therapeutic perspectives |
| Q51736469 | N-Oleoyl-glycine reduces nicotine reward and withdrawal in mice. |
| Q42254106 | Neural Representations of Unconditioned Stimuli in Basolateral Amygdala Mediate Innate and Learned Responses |
| Q34012381 | Neurobiological mechanisms involved in nicotine dependence and reward: participation of the endogenous opioid system |
| Q28111991 | New mechanisms and perspectives in nicotine withdrawal |
| Q45763902 | Nicotine reinforcement is reduced by cannabinoid CB1 receptor blockade in the ventral tegmental area. |
| Q50676331 | Nicotine self-administration induces CB1-dependent LTP in the bed nucleus of the stria terminalis. |
| Q44793980 | Nicotine-induced neuroprotection against ischemic injury involves activation of endocannabinoid system in rats |
| Q37304747 | Peroxisome proliferator-activated receptor (PPAR) agonists as promising new medications for drug addiction: preclinical evidence |
| Q35779281 | Phasic D1 and tonic D2 dopamine receptor signaling double dissociate the motivational effects of acute nicotine and chronic nicotine withdrawal |
| Q37106501 | Rodent models of nicotine reward: what do they tell us about tobacco abuse in humans? |
| Q30551483 | Role of CB2 cannabinoid receptors in the rewarding, reinforcing, and physical effects of nicotine |
| Q35216481 | Role of the endogenous cannabinoid system in nicotine addiction: novel insights |
| Q41489097 | THC reduces the anticipatory nucleus accumbens response to reward in subjects with a nicotine addiction. |
| Q40446321 | The CB1 Neutral Antagonist AM4113 Retains the Therapeutic Efficacy of the Inverse Agonist Rimonabant for Nicotine Dependence and Weight Loss with Better Psychiatric Tolerability. |
| Q50226059 | The Endocannabinoid System as Pharmacological Target Derived from Its CNS Role in Energy Homeostasis and Reward. Applications in Eating Disorders and Addiction. |
| Q33703839 | The cannabinoid CB2 receptor is necessary for nicotine-conditioned place preference, but not other behavioral effects of nicotine in mice |
| Q37291517 | The endocannabinoid system: a new molecular target for the treatment of tobacco addiction. |
| Q34282073 | The role of fatty acid amide hydrolase inhibition in nicotine reward and dependence |