neuropeptide-y and Stress-Disorders--Traumatic

Neuropeptides such as neuropeptide Y (NPY) and corticotropin-releasing hormone (CRH) have been implicated not only in acute regulation of stress/anxiety-related behaviors, but adaptations and changes in these neuropeptide systems may also participate in the regulation of behavior and endocrine responses during chronic stress. NPY is an endogenous anxiolytic neuropeptide, while CRH has anxiogenic properties upon central administration. Changes in these neuropeptide systems may contribute to disease states and give us indications for putative treatment targets for stress/anxiety disorders as well as alcohol/drug dependence. In this review, we briefly present these two systems and review their involvement in mediating the responses to acute and chronic stressors, as well as their possible roles in the development and progression of stress/anxiety disorders. We suggest that neuropeptides may be attractive in treatment development for stress/anxiety disorders, as well as for alcohol/drug dependence, based on their specificity and activity following exposure to external challenges, i.e. stressors, and their differential adaptations during transition from an acute to a chronic stress exposure state.

Topics: Animals; Anxiety; Brain; Corticotropin-Releasing Hormone; Humans; Models, Neurological; Neuropeptide Y; Stress Disorders, Traumatic; Stress, Physiological

Topics: Animals; Biomarkers; Humans; Neuropeptide Y; Stress Disorders, Post-Traumatic; Stress Disorders, Traumatic

Neuropeptide Y (NPY) is a 36-amino acid peptide which exerts several regulatory actions within peripheral and central nervous systems. Among NPY actions preclinical and clinical data have suggested that the anxiolytic and antidepressant actions of NPY may be related to its antagonist action on the hypothalamic-pituitary-adrenal (HPA) axis. The neurotrophins brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) are proteins involved in the growth, survival and function of neurons. In addition to this, a possible role of neurotrophins, particularly BDNF, in HPA axis hyperactivation has been proposed. To characterize the effect of NPY on the production of neurotrophins in the hypothalamus we exposed young adult rats to NPY intraperitoneal administration for three consecutive days and then evaluated BDNF and NGF synthesis in this brain region. We found that NPY treatment decreased BDNF and increased NGF production in the hypothalamus. Given the role of neurotrophins in the hypothalamus, these findings, although preliminary, provide evidence for a role of NPY as inhibitor of HPA axis and support the idea that NPY might be involved in pathologies characterized by HPA axis dysfunctions.

Topics: Animals; Antidepressive Agents; Brain-Derived Neurotrophic Factor; Down-Regulation; Enzyme-Linked Immunosorbent Assay; Hypothalamo-Hypophyseal System; Injections, Intraperitoneal; Male; Nerve Growth Factor; Neuropeptide Y; Pituitary-Adrenal System; Rats; Rats, Wistar; Stress Disorders, Traumatic; Up-Regulation