Modulation of neuropeptide Y levels is impaired in crack withdrawal patients

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.

Neurohormonal changes in medical students during academic srtess

Academic stress is a good model of psychological stress in humans and is thus useful for studying psychoneurohormonal changes. The aim of the current study was to examine the effect of academic examination stress on activation of the hypothalamus-autonomic nervous system [HANS] and the hypothalamic-pituitary-adrenocortical [HPA] axis, through the measurements of changes in neuro-hormones during final exams as compared to the pre-exam baseline. Forty-eight first- and second-year female medical students participated. Plasma leptin, neuropeptide Y [NPY], nitrite, nitrate, andrenomedullin, cortisol and adrenocorticotropic hormone [ACTH] were measured at baseline and during final examinations. Plasma levels of cortisol, ACTH, NPY, adrenomedullin, nitrite and nitrate increased during times of academic stress as compared to baseline levels. However, only plasma leptin level was decreased during the academic stress as compared to baseline, probably through a negative feedback mechanism resulting from sympathetic stimulation. The results indicate that both the HANS and HPA are involved in this type of stress and both are activated at the same time. Academic stress induced significant neurohormonal changes. Leptin, NPY, nitrite, nitrate, adrenomedullin, cortisol and ACTH can be considered part of a complex mosaic model of the neuroendocrine system during academic stress

Neuropeptide Y: a modulator of apoptosis in systemic lupus erythematosus

Systemic lupus erythematosus [SLE] is a multisystem disease characterized by the production of pathological autoantibodies and altered humoral and cellular immune responses. The death receptor Fas is known to induce apoptosis upon interaction with its ligand with consequent activation of caspases and is reported to have an important role in the pathogenesis of SLE. Recently, it has been reported that the nervous system interacts with and directly modulates the immune response through the production of certain neuropeptides as neuropeptide Y [NPY]. To assess the serum level of NPY in SLE patients and to investigate its correlation with the activity of the disease, the level of Fas expression on mononuclear cells and the incidence of apoptosis in SLE patients. The study was conducted on 20 SLE patients and 10 healthy controls. Fas expression was assessed with flow cytometry using mouse antihuman FITC conjugated anti-CD95. The% of apoptotic cells was assessed after cell culture with flow cytometry using propidium iodide staining. NPY was assessed with competitive radioimmunoassay kit for both patients and controls. Both Fas and NPY levels were found to be significantly elevated in SLE as compared with healthy controls [p< 0.01]. Moreover, both levels were found to correlate significantly with the activity score of the disease and with each other. However, despite the elevated Fas expression, the% of apoptotic cells are not significantly increased in SLE compared to healthy controls. Fas expression could be considered a marker of lymphocyte activation in SLE. The presence of high levels of neuropeptides as NPY reflects the link between nervous and immune system. NPY could play an important role as endogenous modulator of the immune response in SLE probably through their inhibiting effect on Fas ligand expression and so switch the lymphocytes to an apoptosis resistant phenotype, which could lead to the activation of autoreactive cells. Thus neuropeptide Y may play an important role in the pathogenesis of SLE