Abstract
Introduction The dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis has a key role in drug addiction susceptibility. In addition to the well-known relationship between cortisol and the HPA axis, other molecules are involved with stress response and could modify the HPA activation, such as the neuropeptide Y (NPY), which has anxiolytic proprieties. There are few studies evaluating the effect of NPY levels on addiction, especially in crack cocaine dependence. Objective To evaluate NPY in crack users during early withdrawal to determine its relationship with drug use and cortisol levels. Methods We analyzed 25 male inpatient crack users. Serum NPY levels were measured at admission and discharge (mean of 24 days). Morning salivary cortisol was measured at admission. Results Serum NPY levels at admission and discharge were very similar. Lower NPY levels at discharge were associated with higher lifetime crack use. Also, a negative correlation was found between morning cortisol and delta NPY (NPY discharge - NPY admission). Conclusion These preliminary findings indicate that crack use influences the modulation of NPY levels and modifies stress response. The NPY pathway may play an important role in the pathophysiology of crack addiction, and the anxiolytic effect of NPY may be impaired in crack users. Future studies should consider NPY as a measurable indicator of the biological state in addiction.
Highlights
The dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis has a key role in drug addiction susceptibility
No influence of recent crack use was detected, a trend towards association was observed between neuropeptide Y (NPY) levels at admission and recent crack use (p = 0.057; Table 2)
The present study shows, for the first time, the influence of crack addiction on NPY levels during early withdrawal
Summary
The dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis has a key role in drug addiction susceptibility. Chronic exposure to drugs of abuse affects the reward system, but evidence showed that other brain systems are deeply involved with addictive behaviors.[1] Dysregulation of the hypothalamic-pituitaryadrenal (HPA) axis plays a key role in drug susceptibility, addiction severity and craving,[2,3] and is involved in stress response. It has been shown that the HPA axis is activated after administration of cocaine, which promotes the release of corticotropinreleasing hormone (CRH), adrenocorticotropic hormone (ACTH) and cortisol.[4] chronic exposure to drugs is associated with attenuated HPA response.[5] Animal models have demonstrated the essential influence of stress on addiction-related outcomes, being associated with increased self-administration of drugs and the reestablishment of drug seeking behavior.[6] the inability to tolerate stress is an important factor that affects drug consumption, relapse and treatment dropout.[7,8]
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