Cortisol as an indicator of dopaminergic effects on nicotine craving

Abstract

There is evidence that glucocorticoids mediate the activity of mesencephalic dopaminergic neurons which play an important role in drug-seeking behaviour and that the absence or presence of glucocorticoids determines the intensity of drug self-administration. Moreover, some experiments indicate that corticoids are increased after substance induced dopaminergic stimulation. These findings could imply (a) that differences in basal glucocorticoid levels are associated with differences in craving or (b) that dopamine (DA) induced corticoid release is an indicator of the sensitivity of the dopaminergic system. Therefore, in a sample of 36 male smokers whose DA system was challenged by a DA agonist (lisuride=LIS) and a DA antagonist (fluphenazine=FLU) in a balanced placebo controlled double-blind crossover design, it was investigated if (a) basal cortisol differences and (b) drug induced cortisol responses are related to the amount of nicotine craving after 3.5 h of deprivation from smoking. There were no differences in craving between subjects with high and low basal cortisol levels irrespective of the pharmacological treatment. However, the size of the cortisol change after the DA challenge and deprivation emerged as a good predictor for the amount of craving in that drug condition in which the cortisol response was most pronounced. Findings were interpreted as evidence for the role of cortisol as an indicator of DA sensitivity.

Blunted opiate modulation of prolactin response in smoking men and women

“…The short-term presence of prolactin abnormalities in blood following cocaine withdrawal show it can be a marker of acute withdrawal (Satel et al, 1991; Buydens-Branchey et al, 1999), and a trend for prolactin dysregulation has been observed with smoking withdrawal (Pickworth et al, 1996). Consistent results from other studies suggest that prolactin dysregulation has a direct relationship with craving and withdrawal (Lee et al, 2005; Reuter and Hennig, 2003). This, combined with previous studies demonstrating the usefulness of measuring peripheral hormonal activity to assess dopaminergic sensitivity (Reuter and Hennig, 2003), indicates that this hormone may be a useful biomarker to consider when investigating stress-related neurobiological dysregulation associated with nicotine dependence.…”

Reduction in Cortisol After Smoking Cessation Among Users of Nicotine Patches

“…The finding of an association between lower cortisol and increased reports of these symptoms is also incongruent with the general finding that cortisol is positively associated with subjective stress (3). It is possible that cortisol mediates the effects of nicotine (14) such that cortisol contributes to the reinforcing properties of cigarettes. Consequently, a sudden decrease in cortisol may cause the smoker distress.…”

“…Cortisol has also been found to downregulate nicotine receptor binding (15); therefore, very low levels of cortisol on the first day of abstinence may result in increased withdrawal symptoms, stress, desire to smoke, and relapse as a result of a rebound effect of increased nicotine receptor sensitivity. Alternatively, some unknown psychosocial or biological factor (e.g., dopamine, see [14]) may simultaneously affect cortisol, urges to smoke, withdrawal symptoms, and stress.…”

“…This effect has been attributed to nicotine exposure (7,8,11,12). Cortisol interacts with several neurotransmitters that mediate the effects of nicotine (e.g., dopamine, ␤-endorphin, acetylcholine [13,14]), and cortisol may be linked to nicotine metabolism in that sensitivity to nicotine tends to be reduced under conditions of enhanced corticosteroid activity (15).…”

A randomised placebo-controlled trial of oral hydrocortisone for treating tobacco withdrawal symptoms

“…The mechanism underlying the observed relationship between a decline in cortisol and increased smoking relapse and withdrawal is unclear. It is possible that low levels of cortisol lead to low mood and craving for cigarettes due to reduced mesolimbic dopamine levels (Reuter and Hennig 2003).…”