Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A historical review is given of the origins of the concepts of negative symptoms. An outline is given of the conceptual difficulties inherent to the negative syndrome, especially influences related to post psychotic depressed patients, neuroleptic treatment and institutionalization are critically reviewed. Subsequently pathophysiological and etiological theories of negative symptoms are reviewed and discussed. The last part of this article contains a discussion of therapeutical strategies in the treatment of negative symptoms. Firstly dopamine agonist strategies are discussed, secondly the role of neuropeptides (vasopressin and TRH) in the treatment of negative symptoms is discussed and a putative therapeutic role for these peptides is suggested.
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PMID:[Negative symptoms and schizophrenia. A concise review of clinical and pharmacotherapeutic data]. 266 3

Directional behavioral and functional asymmetries (i.e., left-biased or right-biased in all or most animals of the population) induced by certain chemical substances are new types of brain and spinal cord asymmetry. The revealed asymmetry comprises: (1) left- or right-biased circle rotation in rat, (2) hind limb postural asymmetry resulting from alteration of the left or right flexion reflex in rat and cat, and (3) asymmetric alterations of the evoked potentials (EP) in the turtle visual cortex. Circle rotation of animals is induced by hypothalamic neurohormones (somatostatin, LH-RH, substance P, and TRH). Postural asymmetry develops under the effect produced by enkephalins and opioid kappa- and delta-agonists, sigma-agonist SKF 10.047, Arg-vasopressin. Endogenous peptide factors, the activity (or content) of which increased under brain and spinal cord unilateral injury, as well as the ones localized in the left or right hemisphere, also induced postural asymmetry. EP of the left and right turtle visual cortex were inhibited by enkephalins and opioid kappa-, and delta- and mu-agonists, and factors predominantly localized in the left or right turtle visual cortex in a different manner. The data reported here suggest the existence of a side-specific mechanism for a selective neurohormonal regulation of the neuronal activity and other processes in the left and right halves of brain and spinal cord which involves lateralized neuropeptides and their receptors. This mechanism might serve to maintain a certain balance between the activity of the left and right-side neurons, and other contralateral processes in the paired and bilateral structures in brain and spinal cord. Significant deviations from the balance occur most likely due to powerful unilateral stimuli, e.g., unilateral trauma. Many neuropeptides (opioid ones, somatostatin, MSH, ACTH) are, presumably, involved in the regeneration processes in the central and peripheral nervous system. In the case of brain lesions, some lateralized endogenous peptides may participate in the regulation of regeneration process on the left, whereas the other ones, on the right side of the midline, which depends on the side of the lesion. Some lateralized receptors and ligands may serve as positional markers of the left, whereas the other ones may serve as those of the right brain hemisphere. In ontogenesis, these markers are probably necessary to perform the function of the mechanism responsible for symmetrical brain formation.
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PMID:Neuropeptides induce directional asymmetry in brain and spinal cord: facts and hypotheses. 268 85

Oxytocin receptors were identified and characterized in bovine mammary tissue. [3H]-oxytocin was specifically bound to the 105,000 X g particulate fractions from 5 lactating cows and 5 non-lactating cows. Binding reached equilibrium by 50 min at 20 degrees C and by 8 hr at 4 degrees C. The half-time of displacement at 20 degrees C was approximately 1 hr. ACTH, TRH, angiotensin I, angiotensin II, pentagastrin, bradykinin, xenopsin and L-valyl-histidyl-L-leucyl-L-threonyl- L-prolyl-L-valyl-L-glutamyl-L-lysine were not competitive in the dose range tested at 20 degrees C. The ability of other peptides to inhibit 3H-oxytocin binding was as follows: oxytocin greater than vasotocin greater than arginine - vasopressin greater than lysine - vasopressin greater than Pen1 Phe2 Thr4 - oxytocin. The Kd of the oxytocin receptor averaged 1.66 +/- 1.19 nMol/L for lactating cows and 0.97 +/- nMol/L for non-lactating cows, respectively. The maximum number of binding sites was 0.14 +/- 0.12 nM/mg protein and 0.15 +/- 0.08 nM/mg protein for lactating cows and non-lactating cows, respectively. Identification and characterization of these receptors now makes it possible to study the dynamics of hormonal binding throughout various physiological states of the animal.
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PMID:Oxytocin receptors in bovine mammary tissue. 282 Dec 49

A 71-year-old man was referred to Tokai University Hospital because of cold intolerance, slow speech and slowing down of his intellectual and motor activities. Free thyroxine index, and free T-4 and T-3 levels were low (1.4, 0.7 ng/dl and 0.4 ng/ml, respectively) with normal TSH (2.5 microIU/ml). A skull X-ray showed enlargement of the sella turcica and his CT scan revealed an intrasellar mass. LH, FSH, ACTH and PRL did not rise in response to the intravenous administration of LH-RH and insulin. A diagnosis of pan-hypopituitarism due to a pituitary tumor was established. The release of ACTH and cortisol was restored under stimulation of CRF or lysine vasopressin. TSH responded to TRH in a delayed manner. The pituitary tumor was removed by a transsphenoidal operation and diagnosed histologically as craniopharyngioma. Our hospital has experienced nine cases of craniopharyngioma in the last 10 years but the present case was the only intrasellar craniopharyngioma.
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PMID:A case of intrasellar craniopharyngioma. 283 33

Thyrotropin releasing hormone (TRH) and its receptors are present in the cardiovascular nuclei of the brain as well as in the intermediolateral cell column of spinal cord. Anatomical, neurophysiological, functional and pharmacological studies suggest that TRH is a neurotransmitter/neuromodulator in the central nervous system. Administration of TRH to experimental animals or human subjects induces pressor and tachycardic responses and increases plasma levels of catecholamines. These effects are likely to be mediated by a central nervous system activation of the sympathoadrenomedullary system with no involvement of vasopressin or renin-angiotensin system. In the conscious rat, the TRH-induced pressor response is accompanied by an increment in cardiac output and a distinct change in organ blood flow, a hindquarter skeletal muscle vasodilation accompanied by renal and mesenteric vasoconstriction. The role of TRH in hypertension has not been studied. However, the extremely potent pressor and vasoconstrictor properties of TRH makes this tripeptide a candidate for neurotransmitters/modulators involved in the development and/or maintenance of hypertension. The role of TRH in the therapy of shock is at present controversial. Though preliminary experimental work raised hopes and expectations for therapeutic usage of TRH in shock and trauma, the more recent studies have shown no effect or a detrimental effect for TRH in some experimental shock states.
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PMID:Cardiovascular pharmacology of thyrotropin releasing hormone. 285 52

The endocrine function of the thyroid and gonads has for long been investigated using the corresponding releasing hormones (TRH- and LHRH-test, respectively). The adrenal cortex has, up to now, been stimulated using insulin-induced hypoglycaemia or lysine-vasopressin and growth hormone stimulated using arginine. New diagnostic possibilities have arisen with the isolation of the corresponding releasing-hormones, CRF and GRF, and with the availability of these too for clinical use. Using the four above mentioned releasing-hormones in a global pituitary-stimulation-test, the secretion of ACTH, cortisol, STH, TSH, LH, FSH and prolactin hormones can now be examined together.
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PMID:[Global pituitary stimulation test with releasing hormones]. 298 36

The effect of neuropeptides and their analogs on anoxia-induced amnesia was examined using one-trial passive avoidance task in mice. Anoxia, produced by the exposure to CO2 immediately after the acquisition of avoidance response, induced amnesia which is shown by a short latency to enter from the safety compartment into the shocked compartment in the retention test conducted 24 hr later. In these anoxia-treated animals, thyrotropin-releasing hormone (TRH: 10-20 mg/kg), its analog DN-1417 (10-20 mg/kg) and ACTH 4-10 (66 micrograms/body), which were given sc 15-60 min before the retention test, markedly prolonged the latency in a dose-dependent manner, indicating a reversal of the amnesia. Arginine- and lysine-vasopressin also reversed the amnesia at a dose of 100 micrograms/body. These results suggest that TRH and DN-1417, known to reverse the amnesia produced by the protein synthesis inhibitor cycloheximide, have ameliorating effects on the retrieval process of memory.
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PMID:[Effect of TRH and its analog DN-1417 on anoxia-induced amnesia in mice]. 299 54

The circulating levels of ACTH and alpha-melanocyte stimulating hormone (alpha-MSH) were measured in 9 patients with Nelson's syndrome after the administration of saline, ovine corticotrophin releasing factor (oCRF), bromocriptine or TRH. The concentrations of ACTH were grossly elevated and alpha-MSH levels ranged from undetectable to higher than the normal range. In seven of eight subjects there was a rapid corticotrophic response, but no change in the alpha-MSH level, following oCRF. This response was delayed in one subject. Following oCRF injection, the plasma oCRF profile was variable but circulating oCRF was detectable even at the end of the experiment in all cases. There was no significant change in circulating ACTH or alpha-MSH following either bromocriptine or TRH. Cultured tumour cells from one case of Cushing's disease showed a corticotrophic response but no change in alpha-MSH to oCRF and the response was enhanced by vasopressin. Bromocriptine added to the same tumour depressed ACTH secretion without affecting the output of alpha-MSH. The present data suggest that the tumours in these subjects are responsive to oCRF and arise from corticotrophs rather than melanotrophs.
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PMID:The effect of ovine corticotrophin releasing factor (oCRF), bromocriptine and TRH on the secretion of ACTH and alpha-MSH in Nelson's syndrome and Cushing's disease. 302 73

CRF stimulates the synthesis and secretion of proopiomelanocortin-derived peptides from AtT-20 mouse pituitary tumor cells. This study has shown that there is a specific binding site for CRF located on the plasma membrane of these cells. Both [125I]iodo-Tyr0CRF and noniodinated CRF (10(-11)-10(-7) M) stimulated, in a dose-dependent manner, the secretion of equimolar amounts of beta-endorphin-like immunoactivity from AtT-20 cells. Disuccinimidyl suberate, a cross-linking agent, was used to demonstrate specific binding of [125I]iodo-Tyr0CRF to plasma membranes from these cells. After cross-linking [125I] iodo-Tyr0CRF, the membrane proteins were solubilized with sodium dodecyl sulfate and electrophoresed on a 10% polyacrylamide gel. A single radioactively labeled band, corresponding to a mol wt of 66,000, was identified by autoradiography. [125I]Iodo-Tyr0CRF binding to these membranes was inhibited by 10(-7) M unlabeled CRF or an equimolar concentration of the CRF analog sauvagine. Similar concentrations (10(-7) M) of TRH, GnRH, insulin, [Arg8]vasopressin, somatostatin, and ACTH did not inhibit [125I]iodo-Tyr0CRF binding to the plasma membranes. Incubation of AtT-20 cells for 24 h in the presence of 10 nM dexamethasone reduced [125I]iodo-Tyr0CRF binding by 80% compared to that in untreated cells. Dexamethasone also inhibited the CRF-stimulated beta-endorphin-like immunoactivity secretory response. These data indicate that binding of CRF to a specific membrane protein is an integral component in the stimulation of AtT-20 cells by CRF.
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PMID:Identification of a corticotropin-releasing factor-binding protein in the plasma membrane of AtT-20 mouse pituitary tumor cells and its regulation by dexamethasone. 303 86

The effect of daily peripheral administration of various peptides on learning and memory performance was studied in male albino rats. Groups of rats were treated with either TRH (1.0 mg/kg) alpha-MSH (1.0 mg/kg), or saline for three days. Other groups were treated either with vasopressin (1.0 microgram/kg) or saline. All treatments were 30 min before testing in a Morris Water Task apparatus. This type of learning is spatial learning which requires integration of environmental cues. Only alpha-MSH treated rats exhibited improved learning on Day 1 and Day 3 of the training period. One month later all rats were retested with no difference between the experimental groups. Single doses of these peptides caused a nonsignificant increase in pain threshold. The body weight gain of vasopressin-treated rats was significantly reduced as well as their motoric behavior. Therefore, the alpha-MSH effect on learning cannot be explained by nonspecific effects on body weight, pain threshold, or motor activity level.
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PMID:Effects of alpha-MSH, TRH and AVP on learning and memory, pain threshold, and motor activity: preliminary results. 311 86


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