Here are some nice nicotine abstracts,not as relevant here with a localized carrier as systematic usage but still good reads.
Nicotine self-administration acutely activates brain reward systems and induces a long-lasting increase in reward sensitivity.
Kenny PJ, Markou A.
Department of Neuropharmacology, The Scripps Research Institute, La Jolla, CA 92037, USA.
Nicotine is a major component of tobacco smoke contributing to the initiation and persistence of the harmful tobacco habit in human smokers. The reinforcing effects of nicotine likely arise through its ability to stimulate brain circuitry mediating the detection and experiencing of natural rewards. Nevertheless, remarkably little is known concerning the acute or long-lasting actions of nicotine on brain reward systems in vivo. Here, we investigated the effects of intravenously self-administered nicotine (0.03 mg/kg/infusion, free base) on the sensitivity of brain reward systems, reflected in alterations of intracranial self-stimulation (ICSS) thresholds in rats. Rats self-administered nicotine during 1 or 12 h daily sessions, with reward thresholds assessed 1 h before and 15 min after each self-administration session. Control rats remained nicotine naïve throughout. Nicotine self-administration increased the sensitivity of brain reward systems, detected by post-nicotine lowering of reward thresholds in 1 and 12 h rats. This nicotine-enhanced sensitivity of reward systems was reversed by the high-affinity nicotinic receptor antagonist dihydro-beta-erythroidine (DHbetaE; 3 mg/kg). Surprisingly, nicotine-induced excitation of reward systems persisted for at least 36 days after nicotine self-administration had ceased. Overall, these data demonstrate that rats can voluntarily consume quantities of nicotine sufficient to increase the sensitivity of brain reward systems, an action likely crucial in establishing and maintaining the nicotine habit. Moreover, self-administered nicotine resets the sensitivity of reward systems to a new increased level, thereby imprinting an indelible 'memory' of its effects in reward systems, an action that so far appears unique to nicotine among drugs of abuse.
Free fulltext:
http://www.nature.com/pdffinder/10.1038/sj.npp.1300905
Nicotine blocks stress-induced decrease in BDNF:
QUOTE
http://cat.inist.fr/?aModele=afficheN&cpsidt=17912073
Titre du document / Document title
Chronic psychosocial stress-induced impairment of hippocampal LTP : Possible role of BDNF
Auteur(s) / Author(s)
ALEISA A. M. ; ALZOUBI K. H. ; GERGES N. Z. ; ALKADHI K. A. ;
Résumé / Abstract
Electrophysiological recording reveals that chronic nicotine treatment prevents stress-induced impairment of long-term potentiation (LTP) in the CA1 region of the hippocampus of anesthetized rats. We investigated the molecular mechanism of this action of nicotine in the CA1 region. Immunoblot analysis showed that chronic nicotine treatment (1 mg/kg, 2 times/day) normalized the stress-induced decrease in the basal levels of BDNF, CaMKII (total and phosphorylated; P-CaMKII), and calmodulin. Additionally, nicotine reversed the stress-induced increase in calcineurin basal levels. Chronic nicotine treatment also markedly increased the basal levels of BDNF in naive rats. Furthermore, high-frequency stimulation (HFS), which increased the levels of P-CaMKII in control as well as nicotine-treated stressed rats, failed to increase P-CaMKII levels in untreated stressed rats. Compared to unstimulated control, the levels of both total CaMKII and calcineurin were increased after HFS in all groups including the stressed, but no changes were detected after HFS in the levels of BDNF and calmodulin. These results indicate that normalization by nicotine of the stress-induced changes in the levels of signaling molecules including BDNF may contribute to the recovery of LTP.
Revue / Journal Title
Neurobiology of disease ISSN 0969-9961
Source / Source
2006, vol. 22, no3, pp. 453-462 [10 page(s) (article)]
Langue / Language
Anglais
Editeur / Publisher
Elsevier, Amsterdam, PAYS-BAS (1994) (Revue)
Mots-clés d'auteur / Author Keywords
Anesthetized rat ; CA1 region ; Calcineurin ; CaMKII ; fEPSP ; Population spike ;
Localisation / Location
INIST-CNRS, Cote INIST : 26483, 35400013887881.0010
Nicotine increases BDNF release:
QUOTE
http://www.sciencedirect.com/science?_ob=A...69ad38690a71c7b
Nicotine regulates SH-SY5Y neuroblastoma cell proliferation through the release of brain-derived neurotrophic factor
Florence Serresa, b, Corresponding Author Contact Information, E-mail The Corresponding Author and Stephen L. Carneyb, 1
aUniversity Department of Pharmacology Oxford University Mansfield Road, Oxford OX1 3QT, UK
bLilly Research Centre Ltd, Sunninghill Road, Surrey GU20 6PH, UK
Accepted 8 May 2006.
Available online 21 June 2006.
References and further reading may be available for this article. To view references and further reading you must purchase this article.
Abstract
Nicotine has been shown to produce some beneficial effects in neurodegenerative disorders, and several studies have suggested that these effects may be mediated in part through the action of the neurotrophic factor BDNF. To further elucidate the interaction between nicotine and BDNF, we examined the effect of nicotine on the proliferation of the neuroblastoma cell line SH-SY5Y, which, following differentiation with retinoic acid, expresses both nicotinic receptors and the receptor for BDNF, TrkB. Both nicotine and the nicotinic alpha-7 selective agonist AR-17779 significantly increased cell proliferation albeit with bell-shaped dose–response kinetics. The blockade of this effect with either the alpha-7 nicotinic antagonist methyllycaconitine or the non-selective nicotinic antagonist mecamylamine indicated that the effect was mediated by nicotinic receptors. Prior addition of neutralising BDNF antibodies or of the tyrosine kinase inhibitor K252A (200 nM) completely blocked nicotine-induced proliferation, suggesting the involvement of TrkB signalling in the mediation of the effect. Nicotine also enhanced both the secretion of BDNF from the SH-SY5Y and cell surface density of TrkB receptors. These effects were abolished by pretreatment with MLA. These data indicate that activation of nicotinic receptors has effects upon the BDNF–TrkB pathway, inducing cell proliferation by promoting the release of BDNF, which in turn activates TrkB receptors.
Keywords: Nicotine; BDNF; TrkB; Growth factor; Methyllycaconitine; Mecamylamine
Chronic nicotine increases (and acute nicotine decreases) hippocampal BDNF:
QUOTE
Acute nicotine decreases, and chronic nicotine increases the expression of brain-derived neurotrophic factor mRNA in rat hippocampus1
Paul J. Kenny2, , a, Sandra E. Filea and Marcus RattrayCorresponding Author Contact Information, E-mail The Corresponding Author, b
a Psychopharmacology Research Unit, Centre for Neuroscience Research, GKT School of Biomedical Sciences, King’s College London, Hodgkin Building, Guy’s Hospital Campus, London SE1 1UL, UK
b Biochemical Neuropharmacology Group, Centre for Neuroscience Research, GKT School of Biomedical Sciences, King’s College London, Hodgkin Building, Guy’s Hospital Campus, London SE1 1UL, UK
Accepted 6 October 2000.
Available online 10 January 2001.
References and further reading may be available for this article. To view references and further reading you must purchase this article.
Abstract
Acute nicotine administration (0.5 mg/kg i.p.) significantly decreased BDNF mRNA levels in dentate gyrus, CA3 and CA1 subfields of the rat hippocampus 2 h and 24 h after administration. However, with 7 days nicotine treatment, tolerance developed to the inhibitory effect of nicotine on BDNF mRNA expression and there was a significant increase in BDNF expression 2 h after the final injection in the CA1 region. These data suggests that changes in expression of hippocampal BDNF may be involved in the behavioural effects of nicotine observed after acute and chronic treatment.
Author Keywords: Neurotrophin; Withdrawal; In situ hybridisation; Acetylcholine; Drug dependence
Neuroscience classification codes: Development and regeneration, Neurotrophic factors: expression and regulation
Repeated nicotine injections actually sensitize D3 neurons in nucleus accumbens (very atypical for reinforcing dopaminergics):
QUOTE
http://biopsychiatry.com/nicotine-dopamined3.htm
Disruption of nicotine conditioning
by dopamine D(3) receptor ligands
by
Le Foll B, Schwartz JC, Sokoloff P
Mol Psychiatry 2003 Feb;8(2):225-30
ABSTRACT
Tobacco smoking is the first cause of preventable death in modern countries. Nicotine replacement therapy or sustained release bupropion helps smoking cessation, but relapse rates are still very high. Nicotine, like other drugs of abuse, activates the dopamine mesolimbic system, which originates in the ventral tegmental area and projects notably to the nucleus accumbens. Situations or environmental stimuli previously associated with cigarette smoking, for example, smell of cigarette smoke, can elicit craving in abstinent smokers and promote relapse. Reducing the effects of nicotine-associated cues might therefore have potential therapeutic utility for smoking cessation. Such an approach has been validated for cocaine in animals, by using the dopamine D(3) receptor-selective partial agonist BP 897, which inhibits cocaine cue-induced drug-seeking behavior. Here we show that rats repeatedly injected with nicotine in a particular environment develop nicotine-conditioned locomotor responses, accompanied by an increase in D(3) receptor expression in the nucleus accumbens. This conditioned behavior was inhibited by BP 897 or a selective D(3) receptor antagonist, suggesting that antagonizing dopamine selectively at the D(3) receptor disrupts nicotine-conditioned effects and might represent a novel therapeutic approach for smoking cessation
