Reward nicotine effects

Lindblom N, de VUliers SH, Semenova S, Kalayanov G, Gordon S, Schilstrom B, Ohansson AM, Markou A, Svensson TH (2005) Active immunisation against nicotine blocks the reward facilitating effects of nicotine and partially prevents nicotine withdrawal in the rat as measured by dopamine output in the nucleus accumbens, brain reward thresholds and somatic signs. Naunyn Schmiedebergs Arch Pharmacol 372 182-194... 

Wise, Roy A., Caterina Marcangione, and Pat Bauco. 1998. "Blockade of the Reward-Potentiating Effects of Nicotine on Lateral Hypothalamic Brain Stimulation by Chlorisondamine" Synapse 29 72-79. 

The various stimulants have no obvious chemical relationships and do not share primary neurochemical effects, despite their similar behavioral effects. Cocaines chemical strucmre does not resemble that of caffeine, nicotine, or amphetamine. Cocaine binds to the dopamine reuptake transporter in the central nervous system, effectively inhibiting dopamine reuptake. It has similar effects on the transporters that mediate norepinephrine and serotonin reuptake. As discussed later in this chapter in the section on neurochemical actions mediating stimulant reward, dopamine is very important in the reward system of the brain the increase of dopamine associated with use of cocaine probably accounts for the high dependence potential of the drug. 

Grottick, A. J., Trube, G., Corrigall, W.A. et al. Evidence that nicotinic alpha(7) receptors are not involved in the hyperlocomotor and rewarding effects of nicotine. J. Pharmacol. Exp. Then 294 1112, 2000. 

Laviolette, S.R., Alexson, T.O., van der Kooy, D. Lesions of the tegmental pedunculopontine nucleus block the rewarding effects and reveal the aversive effects of nicotine in the ventral tegmental area. J. Neurosci. 22 8653, 2002. 

Berrendero, R., Kieffer, B., Maldonado, R. Attenuation of nicotine-induced antinociception, rewarding effects and dependence in mu-opioid receptor knock out mice. J. Neurosci. 22 10935, 2002. 

Inhaled nicotine is efficiently delivered to the brain (see chapter by Benowitz, this volume) where it selectively interacts with its central targets, the neuronal nicotinic acetylcholine receptors (nAChRs). The multiple subtypes of uAChR (see chapter by Collins et al, this volume) all bind nicotine but with different affinities, depending on the subunit composition of the uAChR. Binding may result in activation or desensitisation of uAChRs, reflecting the temporal characteristics of nicotine dehvery and local concentration of nicotine. Another level of complexity of the actions of nicotine reflects the widespread and non-uniform distribution of uAChR subtypes within the brain, such that nicotine can influence many centrally regulated functions in addition to the reward systems. In this chapter, we address the consequences of nicotine interactions with nAChRs at the molecular, cellular and anatomical levels. We critically evaluate experimental approaches, with respect to their relevance to human smoking, and contrast the acute and chronic effects of nicotine. 

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