Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Concentrations of Neuropeptide Y-like (NPY-LI) immunoreactivity in cerebrospinal fluid (CSF) were measured in a group of depressed patients (n = 24) and compared with that of control subjects (n = 12). CSF-NPY-LI was significantly reduced in the group of non-endogenously depressed patients when classified according to Newcastle Rating Scale for Depression--1971 (N-II). No significant correlation was found in the control or depressed groups between lumbar concentrations of NPY-LI and a number of other neurotransmitters.
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PMID:Cerebrospinal fluid concentrations of neuropeptide Y in depressed patients and in controls. 134 25

Neuropeptide Y (NPY) was continuously administered to Wistar rats intracarotidly via the external carotid artery and local cerebral blood flow (LCBF) was measured by a quantitative autoradiography using [14C]iodoantipyrine. A remarkable reduction in LCBF was observed in the NPY infused hemisphere. This depression was irregular and was particularly evident in the hippocampus, selective thalamic nuclei and the cerebral cortex.
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PMID:Effects of intracarotid infusion of neuropeptide Y on cerebral blood flow in rats. 157 93

Neuropeptide Y (NPY) was measured in postmortem brain tissue from victims of suicide and from individuals dying a sudden natural or accidental death (controls). Concentrations of NPY-immunoreactivity were measured by radioimmunoassay in frontal cortex (BA 10), temporal cortex (BA 22), caudate nucleus, and cerebellum. Concentrations of NPY-immunoreactivity were significantly lower in postmortem frontal cortex (-14%) and caudate nucleus (-27%) from suicide victims compared with age-matched controls. A subgroup of suicides with evidence of a history of depression revealed more robust reductions in concentrations of NPY-immunoreactivity in frontal cortex and caudate nucleus, as did four individuals who died from natural causes and also were described as having a possible history of depression. Concentrations of NPY-immunoreactivity in temporal cortex and cerebellum from victims of suicide or from the subgroup of subjects with a possible history of depression were not significantly different from those of age-matched controls. We suggest there is a deficit in the brain NPY system leading to region-specific reductions in peptide concentrations in subjects who have a history of depression.
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PMID:Reduced neuropeptide Y concentrations in suicide brain. 161 14

Neuropeptide Y (NPY) is found to be costored with norepinephrine (NE) in vesicles of the nerve terminals. An endogenous inhibitor of dopamine-beta-hydroxylase (DBH), the synthetic enzyme of NE, has been mentioned. In an attempt to clarify the effect of NPY on DBH activities, an in vitro assay is carried out using chromatographic analysis of NE formation from dopamine. NPY (20-80 pmol/ml) produced a dose-dependent depression of NE formation catalysed by the purified bovine adrenal DBH. Lineweaver-Burke plots (Km = 1.1 mM, Vmax = 10 pmol/min/mg protein) showed a non-competitive inhibition in NPY (30 pmol/ml, IC50)-treated samples. Moreover, failure of denatured NPY even at maximum concentration to influence the DBH activities suggested the essential of natural form of NPY. Participation of sulfhydryl compound seems also negligible, because N-ethylmaleimide did not overcome the effect of NPY. These results indicate that NPY has the ability to inhibit the catalytic action of DBH.
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PMID:Inhibitory effect of neuropeptide Y (NPY) on the in vitro activity of dopamine-beta-hydroxylase. 163 65

The sensitivity of human melanoma and lung cancer strains transplanted to nude mice to the synthetic hormone of hypothalamus--melanostatin has been defined. Correlation has been noted between the rate of melanoma growth inhibition, decrease in the rate of Na-fluorescent accumulation in the tumor and the tendency towards depression of the activity of energetic metabolism enzymes (SDH and alpha-GPDH) in the treated tumors as compared to control. Moderate lymphopenia and absence of effect on the same enzymes of the lymphocytes was also observed. Fluorescent probes can be used in the estimation of the drug action on the tumor and organs.
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PMID:[The action of hypothalamic hormone on athymic mice with transplantable strains of human tumors]. 290 87

Experiments on cats revealed an emotiotropic action of melanostatin on the original spectrum of emotional reactivity, similar to the effects of L-DOPA and amantadin. The drug does not possess an antidepressant action proper but activates the aggressive-defensive behaviour in experimental reserpine depression and reduces the provocation-induced aggressive behaviour in experimental haloperidol depression. In reserpinized mice, it antagonizes reserpine hypothermia, increases muscle tone and eliminates ptosis. It decreases haloperidol-induced catalepsia. Melanostatin increases the brain level of dopamine and its metabolite, homovanilic acid.
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PMID:[Psychopharmacologic spectrum of melanostatin]. 610 96

We examined the effects of intrathecally administered neuropeptide Y on the spinal nociceptive flexor reflex in decerebrate, spinalized, unanesthetized rats with intact sciatic nerves, or 11-39 days after unilateral transection of the sciatic nerve. In rats with intact sciatic nerve, intrathecal neuropeptide Y at low doses (10 and 100 ng) caused a brief facilitation of the flexor reflex. At a dose of 300 ng, the effect of neuropeptide Y on the flexor reflex was biphasic, i.e. a brief facilitation followed by slight depression. At higher doses (1 and 10 micrograms), the effect of neuropeptide Y was mainly inhibitory, causing substantial and usually prolonged depression of the flexor reflex magnitude. The reflex depression caused by intrathecal neuropeptide Y was not reversed by the opioid antagonist naloxone or the alpha 2 adrenoceptor antagonist atipamezole. Intrathecal neuropeptide Y at doses up to 1 and 10 micrograms had no effect on reflex facilitation caused by conditioning stimulation of C-fibers, intrathecal substance P or neurokinin A. Topical application of neuropeptide Y (1 microgram/microliter) failed to influence the monosynaptic reflex in normal rats. Eleven to 16 days after peripheral axotomy, the initial excitation of the flexor reflex to intrathecal neuropeptide Y was significantly enhanced in axotomized compared with normal rats. However, the depressive effect of neuropeptide Y on the flexor reflex was unchanged. Neuropeptide Y did not influence the monosynaptic reflex in axotomized rats at this period. In experiments performed on rats in which the sciatic nerve had been transected 31-39 days previously, the facilitatory effect of neuropeptide Y on the flexor reflex remained enhanced compared with normal rats. Furthermore, the inhibitory effect of neuropeptide Y also increased as 100 ng intrathecal neuropeptide Y was able to produce reflex depression in a similar fashion as 300 ng neuropeptide Y normally and the reflex depression caused by 1 microgram neuropeptide Y was stronger and longer lasting than in normal rats. Intrathecal neuropeptide Y (100 ng-10 micrograms) in rats with intact sciatic nerves caused a moderate decrease in spinal cord dorsal surface blood flow as measured with a laser Doppler flowmeter. This effect of neuropeptide Y was unchanged in axotomized rats. The present results support previous observations that spinal application of neuropeptide Y in normal rats caused antinociception. As the depressive effect of neuropeptide Y is independent of spinal opioid and alpha 2-adrenergic systems, it may be mediated by its own receptors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The effects of intrathecal neuropeptide Y on the spinal nociceptive flexor reflex in rats with intact sciatic nerves and after peripheral axotomy. 753 84

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 (NPY) is found to be costored with norepinephrine (NE) in vesicles of the nerve terminals. Tyrosine hydroxylase (TH), the synthetic enzyme of NE, has been mentioned to be a rate-limiting step. In an attempt to understand the effect of NPY on TH activities, an in vitro assay is carried out using chromatographic analysis of 3,4-dihydroxyphenylalanine (DOPA) formation from tyrosine. NPY (40-120 pmol/ml) produced a dose-dependent depression of DOPA formation catalysed by the adrenal TH of rats. Lineweaver-Burk plot (Km = 156 microM, Vmax = 1.05 nmol/h/mg protein) showed a non-competitive inhibition in NPY (80 pmol/ml, IC50)-treated samples. Moreover, failure of denatured NPY even at maximum concentration to influence the TH activities suggested the essential of nature form for NPY. Participation of pterine cofactor seems also negligible, because increase of 2-amino-4-hydroxy-6,7-dimethyltetrahydropteridine did not overcome the effect of NPY. These results indicate that NPY has the ability to inhibit the catalytic action of TH in the adrenal gland of rats.
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PMID:Inhibitory effect of neuropeptide Y (NPY) on the in vitro activity of tyrosine hydroxylase. 790 29

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


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