Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuropeptide Y-like immunoreactivity (NPY-li) was measured in CSF of 35 drug-free chronic schizophrenic patients. Compared to a group of drug-free controls, CSF NPY-li was significantly higher in these patients. CSF NPY-li decreased with age and longer duration of illness. Measures of structural brain abnormalities on CT scans were significantly associated with lower CSF NPY-li. Relationships between NPY-li and schizophrenic behavior, i.e. positive symptoms, were observed only in the clinically stable (nonrelapsed) drug-free patients. In 31 of the patients CSF was obtained before and after withdrawal from haloperidol maintenance treatment. This withdrawal from haloperidol treatment was associated with a significant increase in CSF NPY-li. There was no significant difference in CSF NPY-li between patients who did and those who did not relapse within 6 weeks following haloperidol withdrawal. The present findings suggest a relationship of CSF NPY-li with various aspects of schizophrenia.
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PMID:Neuropeptide Y-like immunoreactivity in schizophrenia. Relationships with clinical measures. 217 1

Neuropeptide Y (NPY)-like and peptide YY (PYY)-like immunoreactivities were measured in cerebrospinal fluid (CSF) from patients with major depressive disorder or schizophrenia and from healthy volunteers without physical or mental illness. NPY-like material was significantly lower (P less than 0.001) in CSF of patients with depressive disorders than in schizophrenic patients or healthy controls. Treatment with the antidepressant, amiflamine, a selective MAO-A inhibitor, did not alter CSF peptide concentrations. In drug-free schizophrenic patients, normal NPY but reduced PYY concentrations in CSF were observed. Treatment with neuroleptics did not affect the levels of NPY or PYY in the CSF. The finding of reduced CSF concentrations of NPY in patients with major depression and of reduced PYY concentrations in schizophrenia may reflect disturbed synthesis, turnover or degradation of the peptides. These findings suggest that the reduced concentrations of NPY or PYY in the CSF may be used as trait markers of the respective illnesses.
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PMID:Neuropeptide Y and peptide YY as possible cerebrospinal fluid markers for major depression and schizophrenia, respectively. 339 12

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.
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PMID:Central nervous system pharmacology of neuropeptide Y. 764 68

Neuropeptide Y is a 36-amino acid peptide that is widely distributed in the brain. Recently, three neuropeptide Y receptor subtypes were discovered with the aid of peptidergic agonist analogs of neuropeptide Y. Many researchers reported that neuropeptide Y might be involved in locomotor activity, eating behavior, stress responses, memory processing, circadian rhythms, blood pressure and neuroendocrine functions. It was also reported to interact with sigma receptor and corticotropin-releasing factor. Clinical evidence suggests that neuropeptide Y might be related to depression, schizophrenia, anorexia nervosa and Alzheimer's disease. In this review, central distribution and receptor subtypes of neuropeptide Y, its physiological action and its levels in cerebrospinal fluid and plasma in psychiatric and neurological illnesses are described.
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PMID:[Neuropeptide Y: psychopharmacological and clinical aspects]. 794 76

sigma Receptors have been implicated in many pharmacological and physiological functions. sigma Receptors were purported to modulate behavioral alteration induced by cocaine and amphetamine, mediate effects of certain atypical antipsychotic agents, affect tonic potassium channels, the PCP/NMDA receptor complex, duodenal bicarbonate secretion, and CRF-induced colonic motility. sigma Receptors were reported to be altered in schizophrenia in certain studies, and up- and downregulations of sigma receptors have been observed in certain conditions. Neuropeptide Y has been shown to modulate the PCP/NMDA receptor complex in both central and gastrointestinal systems via sigma receptors. sigma Receptors are G-protein linked, and certain actions of sigma receptor ligands were affected by G-protein-modifying agents. Using photoaffinity labeling technique, a polypeptide of about 26 kDa has been identified as a sigma receptor. However, the exact biochemical relationship of this polypeptide to sigma receptors is unknown at present.
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PMID:Delineating biochemical and functional properties of sigma receptors: emerging concepts. 810 75

Neuropeptide concentrations were determined in the postmortem cerebral cortex from 19 cognitive-impaired schizophrenics, 4 normal elderly subjects, 4 multi-infarct dementia (MID) cases, and 13 Alzheimer's disease (AD) patients. Only AD patients met criteria for AD. The normal elderly and MID cases were combined into one control group. Somatostatin concentrations were reduced in both schizophrenia and AD. Neuropeptide Y concentrations were reduced only in schizophrenia, and corticotropin-releasing hormone concentrations were primarily reduced in AD. Concentrations of vasoactive intestinal polypeptide and cholecystokinin also were reduced in schizophrenia, although not as profoundly as somatostatin or neuropeptide Y. In AD, cholecystokinin and vasoactive intestinal peptide were unchanged. Neuropeptide deficits in schizophrenics were more pronounced in the temporal and frontal lobes than in the occipital lobe. The mechanisms underlying these deficits in schizophrenia and AD are likely distinct. In schizophrenia, a common neural element, perhaps the cerebral cortical gaba-aminobutyric acid (GABA)-containing neuron, may underlie these deficits.
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PMID:Neuropeptide deficits in schizophrenia vs. Alzheimer's disease cerebral cortex. 871 4

Neuropeptide Y (NPY) has an important role in the regulation of stress responses and feeding behaviour. There is evidence that some effects elicited by NPY occur due to modulation of action of regular neurotransmitters. The main objective of the present study was to test behavioural effects of the novel neuropeptide Y (NPY) Y(1) receptor antagonist (R)-N-[[4-(aminocarbonylaminomethyl)-phenyl]methyl]-N(2)-(diphe nylacetyl)-argininamide trifluoroacetate (BIBO 3304) on dopamine-dependent behaviour. Intracerebroventricular administration of BIBO 3304 (1, 10, 50 nmol) had no effect on locomotor activity as measured by number of rearings and number of squares visited in an open field test in rats, but at 50 nmol dose defecation was significantly increased. BIBO 3304 (10 nmol) reduced amphetamine-induced increases in horizontal and vertical activity whereas its S-configurated enantiomer BIBO 3457 was inactive. In an open field test BIBO 3304 (10 nmol) inhibited purposeless running in rats sensitized to direct dopaminergic agonist apomorphine (0.5 mg/kg, s.c.). BIBO 3304 (10 nmol but not 1 nmol, i.c.v.) reduced fighting in apomorphine-induced aggression paradigm. Apomorphine-induced aggression was reduced by another, structurally similar, but less potent NPY Y(1) receptor antagonist BIBP 3226 (10 nmol, i.c.v.). A lower dose of BIBP 3226 (1 nmol, i.c.v.) was inactive. Concomitant administration of BIBO 3304 (10 nmol) with low doses of apomorphine (0.5 mg/kg s.c.) over the course of 10 days failed to prevent the development of apomorphine-induced aggressiveness. These data demonstrate that behavioural response to indirectly (amphetamine) and directly (apomorphine) acting dopaminergic stimulants is inhibited by NPY Y(1) receptor antagonists and suggest that NPY Y(1) receptor activation might be important in pathophysiology of disorders associated with hyperactivity of dopaminergic pathways, such as psychosis, schizophrenia and drug abuse. We propose that the effects of BIBO 3304 on amphetamine/apomorphine-induced locomotion and apomorphine-induced aggressiveness are due to modulation of postsynaptic dopaminergic responses rather than direct effects of NPY Y(1) receptor antagonists on dopamine or NPY release.
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PMID:Inhibition of amphetamine- and apomorphine-induced behavioural effects by neuropeptide Y Y(1) receptor antagonist BIBO 3304. 1076 Mar 71

The present review summarizes the findings on the role of neuropeptides in the pathophysiology of schizophrenia and major depression. Several neuropeptides as vasopressin and endorphins in particular, beta-endorphin and gamma-type endorphins, cholecystokinin (CCK), neurotensin, somatostatin and Neuropeptide Y have been implicated in schizophrenia. During the last decade, however, few attempts to explore the significance of most of these and other neuropeptides in the pathophysiology of the disease or their therapeutic potential are found in the literature. An exception is neurotensin, which exerts neuroleptic-like effects in animal studies, while CSF, brain and blood studies are inconclusive. Things are different in major depression. Here much attention is paid to the endocrine abnormalities found in this disorder in particular the increased activity of the hypothalamic-pituitary-adrenal (HPA) axis. Neuropeptides as corticotropin-releasing hormone (CRH), vasopressin and corticosteroids are implicated in the symptomatology of this disorder. As a consequence much work is going on investigating the influence of CRH and corticosteroid antagonists or inhibitors of the synthesis of corticosteroids as potential therapeutic agents. This review emphasizes the role of vasopressin in the increased activity of the HPA axis in major depression and suggests exploration of the influence of the now available non-peptidergic vasopressin orally active V1 antagonists.
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PMID:Neuropeptides involved in the pathophysiology of schizophrenia and major depression. 1275 59

Neuropeptide Y (NPY) plays a role in a variety of basic physiological functions and has also been implicated in regulating cognition, including learning and memory. A decrease in neocortical NPY has been reported for Alzheimer's disease, schizophrenia, bipolar disorder, and depression, potentially contributing to associated cognitive deficits. The goal of the present analysis was to examine variation in neocortical NPY-immunoreactive axon and varicosity density among haplorhine primates (monkeys, apes, and humans). Stereologic methods were used to measure the ratios of NPY-expressing axon length density to total neuron density (ALv/Nv) and NPY-immunoreactive varicosity density to neuron density (Vv/Nv), as well as the mean varicosity spacing in neocortical areas 10, 24, 44, and 22 (Tpt) of humans, African great apes, New World monkeys, and Old World monkeys. Humans and great apes showed increased cortical NPY innervation relative to monkey species for ALv/Nv and Vv/Nv. Furthermore, humans and great apes displayed a conserved pattern of varicosity spacing across cortical areas and layers, with no differences between cortical layers or among cortical areas. These phylogenetic differences may be related to shared life history variables and may reflect specific cognitive abilities.
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PMID:Humans and great apes share increased neocortical neuropeptide Y innervation compared to other haplorhine primates. 2461 88

Neuropeptide Y (NPY) has been found to play a critical role in various mental functions as a neurotransmitter and is involved in the development of schizophrenia, a particularly intractable psychiatric disease whose precise etiology remains unknown. Recent molecular biological investigations have identified several candidate genes which may be associated with this disease, including disrupted-in-schizophrenia 1 (DISC1). The role of DISC1 would involve neurogenesis and neuronal migration. However, the functional consequences of this gene defect have not yet been fully clarified in neuronal systems. In the present study, to clarify the neuropathological changes associated with the function of DISC1, we explored how DISC1 dysfunction can induce abnormalities in the NPY neuronal network in the central nervous system. We performed immunohistochemical analyses (including the observation of the distribution and density) of prefrontal cortex specimens from DISC1-knockout (KO) mice, which are considered to be a novel animal model of schizophrenia. We then evaluated the number and size of NPY-immunoreactive (NPY-IR) neurons and the length of NPY-IR fibers. The number of NPY-IR neurons and the length of the fibers were decreased in the prefrontal cortex of DISC1-KO mice. The decrease was particularly prominent in the superficial regions, and the distribution of NPY-IR neurons differed between wild-type and DISC1-KO mice. However, the size of the neurons in the cortices of the DISC1-KO and wild-type mice did not differ markedly. Our findings suggest that dysfunction of DISC1 may lead to the alteration of NPY neurons and neurotransmission issues in NPY-containing neuron systems, which seem to play important roles in both the mental function and neuronal development. DISC1 dysfunction may be involved in the pathogenesis of schizophrenia through the impairment of the NPY neuronal network.
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PMID:Neuropeptide Y neuronal network dysfunction in the frontal lobe of a genetic mouse model of schizophrenia. 2807 91


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