| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| C Reavill, I P Stolerma. Interaction of nicotine with dopaminergic mechanisms assessed through drug discrimination and rotational behaviour in rats. Journal of psychopharmacology (Oxford, England). vol 1. issue 4. 2012-10-02. PMID:22159140. |
the dopamine antagonists haloperidol and sch 23390 attenuated the discriminative stimulus effect of nicotine and reduced overall rates of responding. |
2012-10-02 |
2023-08-12 |
rat |
| C Reavill, I P Stolerma. Interaction of nicotine with dopaminergic mechanisms assessed through drug discrimination and rotational behaviour in rats. Journal of psychopharmacology (Oxford, England). vol 1. issue 4. 2012-10-02. PMID:22159140. |
there was partial generalization from nicotine to the dopamine d-1 agonist skf 38393. |
2012-10-02 |
2023-08-12 |
rat |
| C Reavill, I P Stolerma. Interaction of nicotine with dopaminergic mechanisms assessed through drug discrimination and rotational behaviour in rats. Journal of psychopharmacology (Oxford, England). vol 1. issue 4. 2012-10-02. PMID:22159140. |
in rats with unilateral, 6-hydroxydopamine lesions of the nigrostriatal dopamine pathway, nicotine produced rotation towards the side of the lesion, a characteristic effect of indirectly acting dopamine agonists such as amphetamine. |
2012-10-02 |
2023-08-12 |
rat |
| Nicotine Blocks Latent Inhibition in Rats: Evidence for Increased Functional Activity of Dopamine in the Mesolimbic System: Peters SL, Gray JA, Joseph MH MRC Brain, Behaviour and Psychiatry Research Group, Department of Psychology, Institute of Psychiatry, London SE5 8AF, UK. Journal of psychopharmacology (Oxford, England). vol 6. issue 1. 2012-10-02. PMID:22291269. |
nicotine blocks latent inhibition in rats: evidence for increased functional activity of dopamine in the mesolimbic system: peters sl, gray ja, joseph mh mrc brain, behaviour and psychiatry research group, department of psychology, institute of psychiatry, london se5 8af, uk. |
2012-10-02 |
2023-08-12 |
rat |
| Joost Wiskerke, Yvar van Mourik, Dustin Schetters, Anton N M Schoffelmeer, Tommy Patti. On the Role of Cannabinoid CB1- and μ-Opioid Receptors in Motor Impulsivity. Frontiers in pharmacology. vol 3. 2012-10-02. PMID:22701425. |
previous studies using a rat 5-choice serial reaction time task have established a critical role for dopamine d2 receptors in regulating increments in motor impulsivity induced by acute administration of the psychostimulant drugs amphetamine and nicotine. |
2012-10-02 |
2023-08-12 |
rat |
| Patricia Mesa-Gresa, Asunción Pérez-Martínez, Rosa Redolat-Iborr. [Nicotine and animal models: what does the environmental enrichment paradigm tell us?]. Adicciones. vol 24. issue 2. 2012-10-01. PMID:22648311. |
we discuss the major changes induced by ee at physical, neurobiological and behavioral levels and review the results of recent studies which indicate that ee promotes both neurochemical (potentiation of the increase in dopamine release induced by nicotine in the brain cortex) and behavioral changes (increased ability to discriminate the presence of reward and decreased impulsivity), thus supporting the hypothesis put forward. |
2012-10-01 |
2023-08-12 |
human |
| Colin S Cunningham, Martin A Javors, Lance R McMaho. Pharmacologic characterization of a nicotine-discriminative stimulus in rhesus monkeys. The Journal of pharmacology and experimental therapeutics. vol 341. issue 3. 2012-09-24. PMID:22438471. |
the current nicotine-discrimination assay did not detect a difference in agonist efficacy between nicotine, varenicline, and cytisine, but did show evidence of involvement of dopamine. |
2012-09-24 |
2023-08-12 |
monkey |
| Jinmin Zhu, Xuan Zhang, Yuehang Xu, Thomas J Spencer, Joseph Biederman, Pradeep G Bhid. Prenatal nicotine exposure mouse model showing hyperactivity, reduced cingulate cortex volume, reduced dopamine turnover, and responsiveness to oral methylphenidate treatment. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 32. issue 27. 2012-09-18. PMID:22764249. |
prenatal nicotine exposure mouse model showing hyperactivity, reduced cingulate cortex volume, reduced dopamine turnover, and responsiveness to oral methylphenidate treatment. |
2012-09-18 |
2023-08-12 |
mouse |
| Jinmin Zhu, Xuan Zhang, Yuehang Xu, Thomas J Spencer, Joseph Biederman, Pradeep G Bhid. Prenatal nicotine exposure mouse model showing hyperactivity, reduced cingulate cortex volume, reduced dopamine turnover, and responsiveness to oral methylphenidate treatment. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 32. issue 27. 2012-09-18. PMID:22764249. |
using a mouse model we show that prenatal nicotine exposure produces hyperactivity, selective decreases in cingulate cortical volume, and radial thickness, as well as decreased dopamine turnover in the frontal cortex. |
2012-09-18 |
2023-08-12 |
mouse |
| Jinmin Zhu, Xuan Zhang, Yuehang Xu, Thomas J Spencer, Joseph Biederman, Pradeep G Bhid. Prenatal nicotine exposure mouse model showing hyperactivity, reduced cingulate cortex volume, reduced dopamine turnover, and responsiveness to oral methylphenidate treatment. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 32. issue 27. 2012-09-18. PMID:22764249. |
a single oral, but not intraperitoneal, administration of a therapeutic equivalent dose (0.75 mg/kg) of methylphenidate decreases the hyperactivity and increases the dopamine turnover in the frontal cortex of the prenatally nicotine exposed mice, once again paralleling the therapeutic effects of this compound in adhd subjects. |
2012-09-18 |
2023-08-12 |
mouse |
| K P Gudehithlu, A-M Duchemin, G A Tejwani, N H Neff, M Hadjiconstantino. Nicotine-induced changes of brain β-endorphin. Neuropeptides. vol 46. issue 3. 2012-09-12. PMID:22483037. |
the acute effect of nicotine on β-endorphin was reversed by the nicotinic antagonist mecamylamine and the dopamine antagonist haloperidol, indicating pharmacological specificity and involvement of dopamine d2-like receptors. |
2012-09-12 |
2023-08-12 |
Not clear |
| Claire Thiriez, Gabriel Villafane, Frédérique Grapin, Gilles Fenelon, Philippe Remy, Pierre Cesar. Can nicotine be used medicinally in Parkinson's disease? Expert review of clinical pharmacology. vol 4. issue 4. 2012-09-04. PMID:22114853. |
however, nicotine may modulate dopamine transmission and has clear motor effects when associated with l-dopa, reducing l-dopa-induced dyskinesias. |
2012-09-04 |
2023-08-12 |
Not clear |
| Sarah E McCallum, Matthew A Cowe, Samuel W Lewis, Stanley D Glic. α3β4 nicotinic acetylcholine receptors in the medial habenula modulate the mesolimbic dopaminergic response to acute nicotine in vivo. Neuropharmacology. vol 63. issue 3. 2012-08-27. PMID:22561751. |
acute nicotine administration increased levels of extracellular dopamine and its metabolites in the nacc. |
2012-08-27 |
2023-08-12 |
rat |
| Sarah E McCallum, Matthew A Cowe, Samuel W Lewis, Stanley D Glic. α3β4 nicotinic acetylcholine receptors in the medial habenula modulate the mesolimbic dopaminergic response to acute nicotine in vivo. Neuropharmacology. vol 63. issue 3. 2012-08-27. PMID:22561751. |
the effect of intra-habenular blockade of α3β4 receptors on nacc dopamine was selective for acute nicotine: neither auib nor 18-mc prevented increases in nacc dopamine stimulated by acute d-amphetamine or morphine. |
2012-08-27 |
2023-08-12 |
rat |
| Lawrence Toll, Nurulain T Zaveri, Willma E Polgar, Faming Jiang, Taline V Khroyan, Wei Zhou, Xinmin Simon Xie, Gregory B Stauber, Matthew R Costello, Frances M Lesli. AT-1001: a high affinity and selective α3β4 nicotinic acetylcholine receptor antagonist blocks nicotine self-administration in rats. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. vol 37. issue 6. 2012-08-14. PMID:22278092. |
these results suggest that its inhibition of nicotine self-administration in rats is not directly due to a decrease in dopamine release from the nac, and most likely involves an indirect pathway requiring α3β4 nachr. |
2012-08-14 |
2023-08-12 |
rat |
| Elizabeth E Van Voorhees, John T Mitchell, F Joseph McClernon, Jean C Beckham, Scott H Kollin. Sex, ADHD symptoms, and smoking outcomes: an integrative model. Medical hypotheses. vol 78. issue 5. 2012-08-09. PMID:22341778. |
on a neurobiological level, the dopamine reward processing system may be implicated in the potentially unique interaction of nicotine with sex and with adhd status. |
2012-08-09 |
2023-08-12 |
Not clear |
| Elizabeth E Van Voorhees, John T Mitchell, F Joseph McClernon, Jean C Beckham, Scott H Kollin. Sex, ADHD symptoms, and smoking outcomes: an integrative model. Medical hypotheses. vol 78. issue 5. 2012-08-09. PMID:22341778. |
specifically, nicotine appears to mitigate core adhd symptoms through interaction with the dopamine reward processing system, and ovarian hormones have been found to interact with nicotine within the dopamine reward processing system to affect neurotransmitter release and functioning. |
2012-08-09 |
2023-08-12 |
Not clear |
| Elizabeth E Van Voorhees, John T Mitchell, F Joseph McClernon, Jean C Beckham, Scott H Kollin. Sex, ADHD symptoms, and smoking outcomes: an integrative model. Medical hypotheses. vol 78. issue 5. 2012-08-09. PMID:22341778. |
based upon this model, the following hypotheses are proposed at the intersection of each of the three variables of sex, adhd, and smoking: (1) individuals with adhd have altered functioning of the dopamine reward system, which diminishes their ability to efficiently form conditioned associations based on environmental contingencies; these deficits are partially ameliorated by nicotine; (2) nicotine interacts with estrogen and the dopamine reward system to increase the positive and negative reinforcement value of smoking in female smokers; (3) in adult females with adhd, ovarian hormones interact with the dopamine reward system to exacerbate adhd-related deficits in the capacity to form conditioned associations; and (4) during different phases of the menstrual cycle, nicotine and ovarian hormones may interact differentially with the dopamine reward processing system to affect the type and value of reinforcement smoking provides for women with adhd. |
2012-08-09 |
2023-08-12 |
Not clear |
| Steven B Harrod, Ryan T Lacy, Jun Zhu, Benjamin A Hughes, Marla K Perna, Russell W Brow. Gestational IV nicotine produces elevated brain-derived neurotrophic factor in the mesocorticolimbic dopamine system of adolescent rat offspring. Synapse (New York, N.Y.). vol 65. issue 12. 2012-07-30. PMID:21990022. |
in this experiment, a novel intravenous (iv) exposure model was used to determine if gestational nicotine (gn) treatment produced alterations in methamphetamine-induced sensitization and the expression of brain-derived neurotrophic factor (bdnf) in the mesocorticolimbic dopamine (da) system of adolescent offspring. |
2012-07-30 |
2023-08-12 |
rat |
| Zheng-Ming Ding, Simon N Katner, Zachary A Rodd, William Truitt, Sheketha R Hauser, Gerald A Deehan, Eric A Engleman, William J McBrid. Repeated exposure of the posterior ventral tegmental area to nicotine increases the sensitivity of local dopamine neurons to the stimulating effects of ethanol. Alcohol (Fayetteville, N.Y.). vol 46. issue 3. 2012-07-30. PMID:22449786. |
repeated exposure of the posterior ventral tegmental area to nicotine increases the sensitivity of local dopamine neurons to the stimulating effects of ethanol. |
2012-07-30 |
2023-08-12 |
rat |