study in cocaine abusers, Wexler et al. (2001) found higher ACC activity both preceding and following the onset of craving while watching a cocaine video, but not when watching happy and sad video tapes, compared to HCs. In addition, cocaine abusers showed lower activation in various prefrontal and temporal areas compared with HCs during the cocaine-cue video. In contrast to Childress et al. (1999), the authors concluded that there was a fundamental neurobiological difference between craving and normal emotional states, most probably due to an imbalance between Inhibitors,research,lifescience,medical limbic and prefrontal cortical activity. During craving, cocaine-dependent subjects showed greater activity than HCs in regions that were found to be active in HCs when viewing sad video tapes compared to happy tapes, suggesting a physiological link between
cocaine cue-responses Inhibitors,research,lifescience,medical and normal dysphoric states rather than normal euphoric states (Wexler et al. 2001). In smokers, greater activation was found after exposure to smoking-related images compared with neutral images in several limbic brain regions (part of the mesocorticolimbic dopamine (DA) reward pathway), as well as in regions part of the visuospatial attention circuitry, compared to HCs (Due et al. 2002). The authors suggest that the reward Inhibitors,research,lifescience,medical and visuospatial attention circuitry act in concert to increase and direct attention to potentially important stimuli, such as smoking stimuli Inhibitors,research,lifescience,medical in deprived smokers (Due et al. 2002). This study thus replicated findings of increased limbic activation during processing of cocaine cues. However,
in comparison to the previous studies performed during craving in abstinent cocaine-dependent individuals, the findings from this study may additionally reflect the effects of craving during acute (nicotine) withdrawal, which might be Inhibitors,research,lifescience,medical different from the effects of craving during long-term abstinence. David et al. (2005) failed to observe significant differences in overall brain activation in a small study with smokers, suggesting Drug_discovery that the absence of whole-brain group differences was due to wide inter-individual variability in magnitude and location of activation, indicating the need for larger sample sizes. In a secondary ROI-analysis, greater ventral striatum/nucleus accumbens (VS/NcA) activation was in smokers, but, however, no correlation was found between NcA activation and selleckchem Veliparib self-reported craving, which might be due to a ceiling effect due to nicotine withdrawal during the study (David et al. 2007). Also, Okuyemi et al. (2006) found significant group (smokers vs. HCs) by condition (smoking vs. neutral) interaction effects in medial PFC, right lateral OFC, and contain bilateral VLPFC activation.