Evidences a(CHEBI:nicotine) to a(CHEBI:dopamine)

However, in rodent and nonprimate animal models, nicotine has been shown to enhance striatal dopamine release and to prevent toxin-induced degeneration of dopaminergic neurons (384, 385).

Nicotine decreases tonic DA release in the striatum that is evoked by single action potentials (127), and nicotine also alters the frequency dependence of DA release that is electrically evoked by stimulus trains (130, 131).

For instance, dopamine increases in the extended amygdala during stress, fear, and nicotine withdrawal (Inglis and Moghaddam, 1999; Pape, 2005; Grace et al., 2007; Gallagher et al., 2008; Koob, 2009; Marcinkiewcz et al., 2009)

Chronic nicotine upregulates alpha4* nAChRs in dopaminergic presynaptic terminals, apparently leading to increased resting dopamine release from those terminals

Nicotine facilitates dopamine release by acting at both somatodendritic and presynaptic nAChRs on mesolimbic246,247 and nigrostriatal247 neurons.

Moreover, (-)-nicotine (indirectly) can produce a release of dopamine in brain regions that are thought to control pleasure and motivation; dopamine is thought to underlie the pleasurable sensations experienced by smokers (e.g., [14, 15] but see [16]).

For example, (-)-nicotine may increase dopamine activity at some brain sites such as the nucleus accumbens, an area thought to be important to drugs of abuse (e.g., [14, 101, 102]; but see [16, 103])

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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.