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Pharmacogenetics. 1998 Apr;8(2):125-8.
Lack of association between the dopamine D2 receptor gene allele DRD2*A1 and cigarette smoking in a United Kingdom population.

Singleton AB, Thomson JH, Morris CM, Court JA, Lloyd S, Cholerton S.

Medical Research Council Neurochemical Pathology Unit, Newcastle General Hospital, Newcastle upon Tyne, UK.

The dopamine D2 receptor gene contains a TaqI repeat fragment length polymorphism creating two alleles DRD2*A1 and DRD2*A2. It has been previously suggested that the lesser allele, DRD2*A1, is more prevalent in individuals who are susceptible to impulsive/addictive/compulsive behaviour, for example, alcoholics, polysubstance abusers and tobacco smokers. We genotyped a series of 104 smokers and 117 non smokers and compared the allele frequencies between the groups. A subset (n = 87) of the smoking population also completed the Classification of Smoking by Motives questionnaire and were given scores for five criteria that drive smoking: automatic, dependence, sedative, stimulant and indulgence. Another subset (n = 52) completed the Fagerstrom Tolerance Questionnaire and were given scores for nicotine dependence. We did not find any increase in allele A1 frequency when comparing smokers to non smokers. Furthermore, neither measure of dependence was affected by possession of the A1 allele; the only difference between DRD2*A1 bearing and DRD2*A2 homozygous individuals in terms of smoking motives was found in the scores for indulgence; the former having a moderately reduced score (by 17%, p < 0.05). We conclude that, in the individuals studied, the dopamine D2 receptor TaqI locus does not affect the drive to smoke. This may be caused by the locus being unrelated to impulsive/addictive/compulsive behaviour, the polymorphism being in linkage disequilibrium with another distinct locus or, alternatively, smoking may represent a behaviour that is not directly comparable to impulsive/addictive/compulsive behaviours previously associated with the DRD2*A1 allele.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10022750&dopt=Abstract

EMBO J. 1999 Mar 1;18(5):1235-44.
Increased neurodegeneration during ageing in mice lacking high-affinity nicotine receptors.

Zoli M, Picciotto MR, Ferrari R, Cocchi D, Changeux JP.

CNRS UA D1284, 'Neurobiologie Moleculaire', Institut Pasteur, 28 rue du Dr Roux, 75724 Paris Cedex 15, France.

We have examined neuroanatomical, biochemical and endocrine parameters and spatial learning in mice lacking the beta2 subunit of the nicotinic acetylcholine receptor (nAChR) during ageing. Aged beta2(-/-) mutant mice showed region-specific alterations in cortical regions, including neocortical hypotrophy, loss of hippocampal pyramidal neurons, astro- and microgliosis and elevation of serum corticosterone levels. Whereas adult mutant and control animals performed well in the Morris maze, 22- to 24-month-old beta2(-/-) mice were significantly impaired in spatial learning. These data show that beta2 subunit-containing nAChRs can contribute to both neuronal survival and maintenance of cognitive performance during ageing. beta2(-/-) mice may thus serve as one possible animal model for some of the cognitive deficits and degenerative processes which take place during physiological ageing and in Alzheimer's disease, particularly those associated with dysfunction of the cholinergic system.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10064590&dopt=Abstract

Cell Immunol. 1999 Feb 25;192(1):48-53.
Effects of cigarette smoking on Fas/Fas ligand expression of human lymphocytes.

Suzuki N, Wakisaka S, Takeba Y, Mihara S, Sakane T.

Departments of Immunology and Medicine, St. Marianna University School of Medicine, Kanagawa, 216-8511, Japan.

Cigarette smoking has been shown to affect human immune responses. We have studied Fas/Fas ligand (FasL) expression, which is involved in the cytotoxic activity, immune privilege, and self-tolerance, and other apoptosis-associated molecule expression of peripheral blood lymphocytes (PBL) in healthy subjects with/without cigarette smoking. We found that expression of FasL protein was detected marginally in the fresh PBL and was induced upon mitogen activation in normal individuals without smoking. In contrast, fresh PBL from those with chronic cigarette smoking exhibited enhanced expression of FasL protein without in vitro mitogen stimulation. Moreover, mitogen stimulation failed to augment FasL protein expression of their lymphocytes, suggesting dysregulation of FasL expression of PBL in individuals with cigarette smoking. In contrast, Fas, Bcl-2, and p53 expression were not significantly different between normal individuals with chronic cigarette smoking and those without smoking. In addition, we found that in vitro brief treatment with nicotine induces and/or enhances FasL mRNA and protein expression of lymphocytes from normal donors without smoking. These results suggest that aberrant FasL expression of lymphocytes is, at least in part, involved in the immune impairment in individuals with chronic cigarette smoking. 1999 Academic Press.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10066346&dopt=Abstract

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