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Nicotine's Effects (nicotine + effects)
Selected AbstractsNeurocognitive variation in smoking behavior and withdrawal: genetic and affective moderatorsGENES, BRAIN AND BEHAVIOR, Issue 1 2009D. E. Evans A burgeoning literature suggests that attentional factors are associated with smoking behavior (e.g. direct nicotine effects and smoking withdrawal). This study examined differences in attentional processing between nonsmokers, satiated smokers and overnight nicotine-deprived smokers by comparing the amplitude of the P300 (P3) component of the event-related brain potential (ERP) elicited during a go,nogo task. We also examined the moderating effects of a common dopamine receptor genotype and state negative affect (SNA) on this ERP index of attention. Nonsmokers relative to smokers had greater nogo P3 amplitude. Carrying the A1 allele at the dopamine receptor D2 (DRD2) Taq1A polymorphism site moderated the effects of withdrawal on nogo P3 amplitude, suggesting the A1 allele is a vulnerability marker for withdrawal-related attentional deficits. Increased SNA also predicted attenuated P3 amplitude among deprived smokers. These findings suggest that DRD2 status and SNA moderate the effects of smoking status and withdrawal on neurocognitive variation during attentional processing. This research contributes to a better understanding of the role of individual differences and attentional processing in smoking behavior. [source] A validated method for the determination of nicotine, cotinine, trans -3,-hydroxycotinine, and norcotinine in human plasma using solid-phase extraction and liquid chromatography-atmospheric pressure chemical ionization-mass spectrometryJOURNAL OF MASS SPECTROMETRY (INCORP BIOLOGICAL MASS SPECTROMETRY), Issue 6 2006Insook Kim Abstract A liquid chromatographic-mass spectrometric method for the simultaneous determination of nicotine, cotinine, trans -3,-hydroxycotinine, and norcotinine in human plasma was developed and validated. Analytes and deuterated internal standards were extracted from human plasma using solid-phase extraction and analyzed by liquid chromatography/atmospheric pressure chemical ionization-mass spectrometric detection with selected ion monitoring (SIM). Limits of detection and quantification were 1.0 and 2.5 ng/ml, respectively, for all analytes. Linearity ranged from 2.5 to 500 ng/ml of human plasma using a weighting factor of 1/x; correlation coefficients for the calibration curves were > 0.99. Intra- and inter-assay precision and accuracy were < 15.0%. Recoveries were 108.2,110.8% nicotine, 95.8,108.7% cotinine, 90.5,99.5% trans -3,-hydroxycotinine, and 99.5,109.5% norcotinine. The method was also partially validated in bovine serum, owing to the difficulty of obtaining nicotine-free human plasma for the preparation of calibrators and quality control (QC) samples. This method proved to be robust and accurate for the quantification of nicotine, cotinine, trans -3,-hydroxycotinine, and norcotinine in human plasma collected in clinical studies of acute nicotine effects on brain activity and on the development of neonates of maternal smokers. Copyright © 2006 John Wiley & Sons, Ltd. [source] REVIEW: Nicotine self-medication of cognitive-attentional processingADDICTION BIOLOGY, Issue 1 2009David E. Evans ABSTRACT This article selectively reviews research concerning nicotine's effects on cognition, including the neurobiological mechanism for these effects, task and experimental features that may be important for elucidating these effects, and why these effects may have amplified motivational significance among smokers with cognitive deficit. Nicotine has effects on various cognitive processes, though most studies in humans have focused on the amelioration of cognitive deficits experienced during drug withdrawal. The direct cognitive-enhancing effect of nicotine remains a controversial topic. The relationship between attentional and non-attentional cognitive effects of nicotine is discussed in the context of cognitive self-medication. Further research should include theory-driven examination of cognitive effects of nicotine, and develop targeted smoking cessation programs based on an improved understanding of the role of cognitive self-medication in high-risk individuals. [source] Alcohol tolerance and nicotine cross-tolerance in adolescent miceADDICTION BIOLOGY, Issue 2 2001Marcelo F. Lopez The present experiment was designed to evaluate the development of tolerance to alcohol and cross-tolerance to nicotine in adolescent mice. C57BL/6J mice (30,40 days old) were injected IP with alcohol (2.5 g/kg) for 4 consecutive days. A control group received four saline injections. On the test day, all subjects received an alcohol injection. Tolerance to alcohol's hypothermic effect was observed. Mice (male and female) exposed to alcohol for the 4 previous days showed less hypothermic response to an alcohol challenge than animals injected for 4 days with saline and then challenged with alcohol. Tolerance to alcohol's motor incoordinating effects and differences in blood alcohol concentrations were not observed. Thirty days following alcohol treatment, the same mice received a single nicotine injection (1 mg/kg) to assess cross-tolerance. Nicotine's effect on locomotor activity (open field test) and rectal temperature varied as a function of prior adolescent alcohol exposure and gender. Specifically, female mice who had been exposed to alcohol administrations were more resistant to nicotine's effect on locomotion and temperature than saline-treated animals. In summary, these data demonstrate that adolescent mice develop tolerance to some, but not all, alcohol-induced responses, and that female mice are cross-tolerant to nicotine's effects on temperature and activity. [source] Colonic motility in chronic ulcerative proctosigmoiditis and the effects of nicotine on colonic motility in patients and healthy subjectsALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 5 2001B. Coulie Background: Nicotine decreases diarrhoea and pain in ulcerative colitis without reducing inflammation. Aims: (i) To evaluate the effect of ulcerative proctosigmoiditis on motor functions of an uninflamed segment of descending colon; and (ii) to assess nicotine's effects on colonic motor functions in patients and healthy subjects. Methods: In healthy subjects (n=30) and patients with ulcerative colitis (13; 11 active, two quiescent colitis), we studied the effects of intravenous nicotine on colonic transit of solid residue by scintigraphy (healthy subjects) and on colonic motility in healthy subjects and 11 patients. Results: In ulcerative colitis, fasting colonic motility was increased, whereas motor response to a meal was significantly reduced; compliance was unchanged. In healthy subjects, high-dose nicotine induced transient high amplitude propagated contractions and relaxation of the descending colon followed by decreased phasic contractions. This dose also accelerated colonic transit. Low-dose nicotine (mimicking a transdermal nicotine patch) reduced colonic compliance in healthy subjects, but did not affect motor function in ulcerative colitis. Conclusions: Ulcerative proctosigmoiditis increases fasting colonic motility and reduces tone response to a meal in the descending colon without affecting colonic compliance, suggesting changes in physiological responses but not intrinsic wall properties. Nicotine has dose-dependent effects on colonic motor activity in healthy subjects. [source] | ||||||||||