Effects of nicotine on the nucleus accumbens and similarity to those of addictive drugs

Abstract

The question of whether nicotine, the neuroactive compound of tobacco, is addictive has been open to considerable scientific and public discussion. Although it can serve as a positive reinforcer in several animal species, including man, nicotine is thought to be a weak reinforcer in comparison with addictive drugs such as cocaine and heroin, and has been argued to be habit forming but not addictive. Here we report that intravenous nicotine in the rat, at doses known to maintain self-administration, stimulates local energy metabolism, as measured by 2-deoxyglucose autoradiography, and dopamine transmission, as estimated by brain microdialysis, in the shell of the nucleus accumbens. These neurochemical and metabolic effects are qualitatively similar to those of other drugs, such as cocaine, amphetamine and morphine, which have strong addictive properties. Our results provide functional and neurochemical evidence that there are specific neurobiological commonalities between nicotine and addictive drugs.

Methylphenidate Enhances the Abuse-Related Behavioral Effects of Nicotine in Rats: Intravenous Self-Administration, Drug Discrimination, and Locomotor Cross-Sensitization

“…Nicotine increases dopaminergic neurotransmission by activation of highaffinity b2 subunit-containing nicotinic cholinergic receptors localized on dopamine cell bodies in the ventral tegmental area (VTA), as well as by altering the tone of g-amino butyric acid and glutamate inputs to the VTA (Mansvelder and McGehee, 2002;Mansvelder et al, 2003); the net effect is an increase in extracellular dopamine levels in the NAcc (Pontieri et al, 1996). In contrast, methylphenidate, a dopamine and norepinephrine transport inhibitor, does not release dopamine directly, but rather prevents dopamine clearance in the NAcc and other corticolimbic structures, thus yielding a net increase in extracellular dopamine in those terminal fields (Grace, 2001).…”

Acute Alcohol Effects on Neuronal and Attentional Processing: Striatal Reward System and Inhibitory Sensory Interactions under Acute Ethanol Challenge

“…Opiate receptors of the m-type are not directly situated on the dopaminergic mesocorticolimbic neurons, but on GABAergic interneurons and GABAergic afferents to the VTA. Stimulation of these receptors leads to inhibition of both tonic and phasic release of GABA, which is secondary followed by disinhibition of dopaminergic VTA neurons (Gysling and Wang, 1983;Dilts and Kalivas, 1989;Pontieri et al, 1996). On the other hand, m opiate receptors are also found on GABAergic neurons of the NA, which receive the dopaminergic projections from the VTA neurons (Dilts and Kalivas, 1989).…”

Effect of Ginseng Saponins on Enhanced Dopaminergic Transmission and Locomotor Hyperactivity Induced by Nicotine

“…Evidence suggests that nicotine, the neuroactive compound of tobacco, has common neurochemical as well as behavioral properties with other addictive drugs such as cocaine and amphetamine (Henningfield and Heishman, 1995;Pontieri et al, 1996). It is well documented that nicotine stimulates dopamine (DA) release in the nucleus accumbens and striatum (Imperato et al, 1986;Damsma et al, 1989;Toth et al, 1992;Benwell and Balfour, 1994;Nisell et al, 1994a;Pontieri et al, 1996;Mirza et al, 1996;Marshall et al, 1997).…”

“…It is well documented that nicotine stimulates dopamine (DA) release in the nucleus accumbens and striatum (Imperato et al, 1986;Damsma et al, 1989;Toth et al, 1992;Benwell and Balfour, 1994;Nisell et al, 1994a;Pontieri et al, 1996;Mirza et al, 1996;Marshall et al, 1997). This property has been related to the addictive and behavioral properties of nicotine (Benwell and Balfour, 1992;Corrigall et al, 1992;Di Chiara and Imperato, 1988).…”