Abstract
IntroductionPerturbations in neural function provoked by a drug are thought to induce neural adaptations, which, in the absence of the drug, give rise to withdrawal symptoms. Previously published structural data from this study indicated that the progressive development of physical dependence is associated with increasing density of white matter tracts between the anterior cingulum bundle and the precuneus.MethodsUsing functional magnetic resonance imaging, we compared 11 smokers after 11 h of abstinence from nicotine and after satiation, with 10 nonsmoking controls, using independent component analysis for brain network comparisons as well as a whole brain resting-state functional connectivity analysis using the anterior cingulate cortex as a seed.ResultsIndependent component analysis demonstrated increased functional connectivity in brain networks such as the default mode network associated with the withdrawal state in multiple brain regions. In seed-based analysis, smokers in the withdrawal state showed stronger functional connectivity than nonsmoking controls between the anterior cingulate cortex and the precuneus, caudate, putamen, and frontal cortex (P < 0.05). Among smokers, compared to the satiated state, nicotine withdrawal was associated with increased connectivity between the anterior cingulate cortex and the precuneus, insula, orbital frontal gyrus, superior frontal gyrus, posterior cingulate cortex, superior temporal, and inferior temporal lobe (P < 0.02). The intensity of withdrawal-induced craving correlated with the strength of connectivity between the anterior cingulate cortex and the precuneus, insula, caudate, putamen, middle cingulate gyrus, and precentral gyrus (r = 0.60–0.76; P < 0.05).ConclusionsIn concordance with our previous report that structural neural connectivity between the anterior cingulate area and the precuneus increased in proportion to the progression of physical dependence, resting-state functional connectivity in this pathway increases during nicotine withdrawal in correlation with the intensity of withdrawal-induced craving. These findings suggest that smoking triggers structural and functional neural adaptations in the brain that support withdrawal-induced craving.
Highlights
Perturbations in neural function provoked by a drug are thought to induce neural adaptations, which, in the absence of the drug, give rise to withdrawal symptoms
diffusion tensor imaging (DTI) indicated that progression along the Levels of physical dependence (PD) corresponds with increased density of white matter tracts between the anterior cingulum bundle (ACb) and the precuneus (r = 0.75, P < 0.05), but decreased density of white matter tracts between the ACb and the white matter approaching the frontal cortex (r = À0.86, P < 0.001). (Huang et al 2013) As these analyses suggested a role for the ACb in the development of PD, and whereas Withdrawal-induced craving (WIC) is the dynamic manifestation of PD, we sought to examine the role of the anterior cingulate cortex (ACC) in WIC
The DTI data from this study revealed that FA was higher in smokers than nonsmokers in the white matter of the ACb, and that FA in this area correlated with the level of PD (r = À0.68) and the Hooked on Nicotine Checklist (HONC) (r = À0.65). (Huang et al 2013) For this reason, and because the ACC has been implicated in drug craving, (Brody et al 2002, 2006; David et al 2005; Lim et al 2005; Wilson et al 2005; Franklin et al 2006; Rubinstein et al 2010) we used the bilateral ACC as the seed for our restingstate functional connectivity (rsFC) analysis
Summary
Perturbations in neural function provoked by a drug are thought to induce neural adaptations, which, in the absence of the drug, give rise to withdrawal symptoms. Conclusions: In concordance with our previous report that structural neural connectivity between the anterior cingulate area and the precuneus increased in proportion to the progression of physical dependence, resting-state functional connectivity in this pathway increases during nicotine withdrawal in correlation with the intensity of withdrawal-induced craving. These findings suggest that smoking triggers structural and functional neural adaptations in the brain that support withdrawal-induced craving. Perturbations in neural function provoked by a drug are thought to induce counter-posing homeostatic neural adaptations, which, in the absence of the drug, give rise to withdrawal symptoms.
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