neuropeptide-y and Mental-Disorders

The brain receives and integrates environmental and metabolic information, transforms these signals into adequate neuronal circuit activities, and generates physiological behaviors to promote energy homeostasis. The responsible neuronal circuitries show lifetime plasticity and guaranty metabolic health and survival. However, this highly evolved organization has become challenged nowadays by chronic overload with nutrients and reduced physical activity, which results in an ever-increasing number of obese individuals worldwide. Research within the last two decades has aimed to decipher the responsible molecular and cellular mechanisms for regulation of the hypothalamic melanocortin neurons, which have a key role in the control of food intake and energy metabolism. This review maps the central connections of the melanocortin system and highlights its global position and divergent character in physiological and pathological metabolic events. Moreover, recently uncovered molecular and cellular processes in hypothalamic neurons and glial cells that drive plastic morphological and physiological changes in these cells, and account for regulation of food intake and energy metabolism, are brought into focus. Finally, potential functional interactions between metabolic disorders and psychiatric diseases are discussed.

Topics: Agouti-Related Protein; Animals; Eating; Energy Metabolism; Humans; Hypothalamus; Melanocortins; Mental Disorders; Models, Neurological; Neuroglia; Neurons; Neuropeptide Y; Organelles; Pro-Opiomelanocortin

Tobacco is a highly addictive drug and is one of the most widely abused drugs in the world. The first part of this review explores the role of stressors and stress-associated psychiatric disorders in the initiation of smoking, the maintenance of smoking, and relapse after a period of abstinence. The reviewed studies indicate that stressors facilitate the initiation of smoking, decrease the motivation to quit, and increase the risk for relapse. Furthermore, people with depression or an anxiety disorder are more likely to smoke than people without these disorders. The second part of this review describes animal studies that investigated the role of brain stress systems in nicotine addiction. These studies indicate that corticotropin-releasing factor, Neuropeptide Y, the hypocretins, and norepinephrine play a pivotal role in nicotine addiction. In conclusion, the reviewed studies indicate that smoking briefly decreases subjective stress levels but also leads to a further dysregulation of brain stress systems. Drugs that decrease the activity of brain stress systems may diminish nicotine withdrawal and improve smoking cessation rates.

Topics: Animals; Corticotropin-Releasing Hormone; Disease Models, Animal; Humans; Hypothalamo-Hypophyseal System; Intracellular Signaling Peptides and Proteins; Mental Disorders; Neuropeptide Y; Neuropeptides; Norepinephrine; Orexins; Pituitary-Adrenal System; Tobacco Use Disorder

Extensive preclinical studies suggest neuropeptide Y (NPY) to be involved in stress regulation and coping. NPY counteracts the behavioral consequences of stress and anxiety to maintain emotional homeostasis. NPY is also involved in learning, memory, and cognition, all of which are dysregulated in many psychiatric states. Dense localization of NPY and NPY receptors is found in brain areas implicated in psychopathology such as the amygdala, hippocampus, neocortex, septum, caudate-putamen, hypothalamus and locus coeruleus. Impaired central NPY signaling may therefore be involved in the pathophysiology of depression, anxiety, schizophrenia, alcoholism, and trauma-induced disorders like PTSD. Studies on the readily accessible plasma from psychiatric patients have provided some information on the relevance of NPY as a marker for sympathetic tone in certain conditions. Reports on cerebrospinal fluid (CSF) NPY in subjects with depression indicate a dysregulation of central NPY in this disorder, however, other conditions still need to be investigated.

Topics: Animals; Humans; Mental Disorders; Neuropeptide Y; Psychiatry

Topics: Alcoholism; Animals; Humans; Mental Disorders; Neuropeptide Y

In the CNS, there are widespread and diverse interactions between growth factors and estrogen. Here we examine the interactions of estrogen and brain-derived neurotrophic factor (BDNF), two molecules that have historically been studied separately, despite the fact that they seem to share common targets, effects, and mechanisms of action. The demonstration of an estrogen-sensitive response element on the BDNF gene provided an impetus to explore a direct relationship between estrogen and BDNF, and predicted that the effects of estrogen, at least in part, might be due to the induction of BDNF. This hypothesis is discussed with respect to the hippocampus, where substantial evidence has accumulated in favor of it, but alternate hypotheses are also raised. It is suggested that some of the interactions between estrogen and BDNF, as well as the controversies and implications associated with their respective actions, may be best appreciated in light of the ability of BDNF to induce neuropeptide Y (NPY) synthesis in hippocampal neurons. Taken together, this tri-molecular cascade, estrogen-BDNF-NPY, may be important in understanding the hormonal regulation of hippocampal function. It may also be relevant to other regions of the CNS where estrogen is known to exert profound effects, such as amygdala and hypothalamus; and may provide greater insight into neurological disorders and psychiatric illness, including Alzheimer's disease, depression and epilepsy.

Topics: Adult; Animals; Brain-Derived Neurotrophic Factor; Central Nervous System; Estrogens; Hippocampus; Humans; Intercellular Signaling Peptides and Proteins; Mental Disorders; Nervous System Diseases; Neuropeptide Y; Steroids

Neuropeptide Y (NPY) is a 36-amino acid peptide belonging to the pancreatic polypeptide family that has marked and diverse biological activity across species. NPY originally was isolated from mammalian brain tissue somewhat more than 10 years ago and, since that time, has been the subject of numerous scientific publications. NPY and its proposed three receptors (Y1, Y2 and Y3) are relatively abundant in and uniquely distributed throughout the brain and spinal cord. This review will highlight the results from a number of research-oriented studies that have examined how NPY is involved in CNS function and behavior, and how these studies may relate to the possible development of medicines, either NPY-like agonists or antagonists, directed towards the treatment of disorders such as anxiety, pain, hypertension, schizophrenia, memory dysfunction, abnormal eating behavior and depression.

Topics: Animals; Central Nervous System; Humans; Mental Disorders; Neuropeptide Y

1. NPY is a 36 amino acid tyrosine-rich peptide. It is one of the most abundant and widely distributed neuropeptides known today within the central nervous system with particularly high concentrations in the hypothalamus and in several limbic regions. 2. NPY seems to coexist with other on neurotransmitters like somatostatin, galanin, GABA and the catecholamines noradrenaline and adrenaline in discrete brain regions. 3. NPY binding sites are widely distributed in the brain. However they do not always overlap with the distribution of NPY-like immunoreactivity. 4. NPY is suggested to be involved in a large number of neuroendocrine functions, stress responses, circadian rhythms, central autonomic functions, eating and drinking behaviour, and sexual and motor behaviour. 5. Psychotropic drugs and neurotoxins can alter the NPY concentrations in discrete brain regions. 6. It is possible that NPY is related to various neurological and psychiatric illnesses, like Huntington's chorea, Alzheimer's disease, Parkinson's disease, eating disorders, and major depressive illness.

Topics: Animals; Central Nervous System; Humans; Mental Disorders; Nervous System Diseases; Neuropeptide Y

In recent decades, the role of genetic factors in the predisposition to suicidal behavior has attracted considerable attention. Although each genetic investigation appears to be valuable, no one study on its own can comprehensively explain the etiology of suicidal behavior.. In this study, using a broad literature review, we found the suicide-associated gene coexpression network. In addition, cytoband, molecular function, biological process, cellular component, tissue-based expression, and disease/disorder enrichment analyses were carried out to determine the most central cellular and molecular infrastructures involved in suicidal behavior.. The reconstructed network consisted of 104 genes, including 91 previously known genes and 13 novel genes, and 354 interactions. Topological analysis showed that in total, CCK, INPP1, DDC, and NPY genes are the most fundamental hubs in the network. We found that suicide genes are significantly concentrated within chromosomes 11 and 6. Further analysis showed that monoaminergic signal transduction, especially through GPCRs, in the cingulate gyrus, superior prefrontal gyrus, dorsal striatum, and the cerebellum are the main, deficient routes in suicide. Moreover, it turned out that genetically, suicidal behavior is more likely in patients with mood and affective disorders.. Like other behavioral disorders, suicide has a complex and multifactorial basis and at present, the only approaches to the integrated study of such disorders are computer-based methods. The results of such studies, although subject to a degree of uncertainty, however, can pave the way for future basic and clinical studies.

Topics: Aromatic-L-Amino-Acid Decarboxylases; Cholecystokinin; Databases, Genetic; Humans; Mental Disorders; Mood Disorders; Neuropeptide Y; Phosphoric Monoester Hydrolases; Risk Factors; Suicidal Ideation; Suicide; Suicide, Attempted