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Query: UNIPROT:P01178 (
oxytocin
)
15,767
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Plasma prolactin, growth hormone, cortisol, luteinising-hormone-releasing hormone (LHRH),
thyrotropin-releasing hormone
(
TRH
), and nicotine and oestrogen stimulated
neurophysin
(NSN and ESN) were measured before and for 6 min after electroconvulsive therapy (ECT) in eight women with severe electroconvulsive therapy (ECT) in eight women with severe depression. Plasma concentrations of NSN and ESN had increased significantly (as much as 10-fold for NSN) within 1 min of the seizure, and concentrations of prolactin had increased within 2-4 min after the seizure. Whereas plasma prolactin and ESN either continued to increase or remained raised throughout the 6 min after seizure, the concentrations of NSN fell to reach a value at 6 min that was approximately 50% of the maximum. There were no increases in any of the other hormones or peptides within the 6 min period under study. Thus ECT has selective effects on hormone release which cannot be attributed simply to a generalised release of pituitary or hypothalamic hormones in response to brain stimulation and/or stress.
...
PMID:Immediate increases in plasma prolactin and neurophysin but not other hormones after electroconvulsive therapy. 612 44
The source and topography of neuropeptide-containing axons in the median eminence are summarized. Several of these neuropeptide-containing neurons (
thyrotropin-releasing hormone
, corticotropin-releasing hormone, vasopressin,
oxytocin
, cholecystokinin) are localized in the paraventricular nucleus. The periventricular and medial preoptic nuclei constitute the main sources of somatostatin and luteinizing hormone releasing hormone axons in the median eminence, respectively. Dynorphins and alpha-neo-endorphin-synthetizing neurons in the supraoptic nucleus also project to the median eminence. Wherever they originate, the projections may follow a common organization pattern and use a common gate--the lateral retrochiasmatic area--to enter the median eminence.
...
PMID:Neuropeptides in the hypothalamo-hypophyseal system: lateral retrochiasmatic area as a common gate for neuronal fibers towards the median eminence. 614 39
The brain contains a large variety and number of peptides some of which were known earlier as hypothalamic hormones (vasopressin,
oxytocin
, luteinizing hormone-releasing hormone,
thyrotropin-releasing hormone
, somatostatin) or as pituitary hormones (the family of opiomelanocortins), while others, not primarily known as hypothalamic or pituitary hormones, may also have endocrine effects (substance P, angiotensin II, neurotensin, bombesin, vasoactive intestinal peptide (VIP), gastrin-cholecystokinin, glucagon, carnosine, bradykinin). These peptides, which form a new class of putative neurotransmitters, are present early in brain development and show important sex differences in both their pattern of innervation and their effects. Their peripheral effects may include intrauterine growth of the placenta and fetus, the timing of birth, acceleration of the course of labour and responses to haemorrhage (redistribution of cardiac output and stimulation of blood cell formation). Endogenous peptides are probably involved in brain development, which may explain their general, permanent and sex-dependent effects when given in the period of rapid brain development. Although peptides might in the future be useful for stimulating recovery from retarded brain development, at present one should be aware of the potential dangers of their use in, for example, obstetrics.
...
PMID:Development of peptidergic systems in the rat brain. 627 64
Isometric tension responses to neuropeptides were recorded from anococcygeus muscles isolated from male mice. This smooth muscle tissue is innervated by inhibitory nonadrenergic, noncholinergic nerves that resemble, ultrastructurally, the peptidergic neurons of the gastrointestinal tract; the physiological function of the anococcygeus is not known. Slow sustained contractions were produced by
oxytocin
(0.2-20 nM), [Arg8]vasopressin (0.4-200 nM), and [Arg]-vasotocin (0.4-100 nM); the mouse anococcygeus is, therefore, one of the few examples of nonvascular smooth muscle from male mammals to respond to low concentrations of
oxytocin
and related peptides. Substance P (0.5-8 microM) caused distinctive, biphasic increases in muscle tone of some, but not all, preparations. Other neuropeptides producing contractions were neurotensin (2-100 microM) and
thyrotropin-releasing hormone
(2-100 microM); the responses were of similar time course and displayed selective cross-desensitization, suggesting that these two peptides act through a common distinct mechanism. Tetradecapeptide somatostatin (10-80 microM) and its analog urotensin II (0.1-5 microM), a dodecapeptide from the urophysis of the teleost fish Gillichthys mirabilis, produced similar slowly developing relaxations of carbachol-induced tone. Piscine urotensin II, of which there are no reported effects on nonvascular mammalian systems, was 20-50 times more potent than somatostatin, a well-established mammalian hormone. Of the peptides studied, only vasoactive intestinal polypeptide (0.05-1 microM) caused rapid powerful relaxations in low concentrations; this is consistent with its proposed involvement in nonadrenergic, noncholinergic neurotransmission in the mouse anococcygeus.
...
PMID:Neuropeptide-induced contraction and relaxation of the mouse anococcygeus muscle. 658 16
The distribution of gonadotropin-releasing hormone (GnRH) was studied in the brain and infundibulum (INF) or median eminence of sheep utilizing a peroxidase-antiperoxidase immunohistochemical method. This procedure utilized a specific antiserum generated against GnRH conjugated to bovine serum albumin. In the rostral INF, the greatest concentration of GnRH positive axons was found in the medial region, mostly in the external layer dorsal to the hypophysial portal plexus. In the intermediate portion of the INF, the hormone was mainly observed in the external layer at the more dorsolateral areas ventral to the tuberoinfundibular sulcus. GnRH was generally located medially in the caudal portion of the INF and dorsomedially in the rostral infundibular stalk. Substantial amounts of reaction product were also noted in the internal layer throughout the entire rostrocaudal extent of the INF. The hormone was localized in axons throughout the brain from the septal and medial preoptic areas to the mammillary bodies. GnRH-positive perikarya were scattered in various regions of the infundibular (arcuate) and for the first time in the ventromedial nuclei of sheep hypothalamus. Preabsorption of the specific antiserum with synthetic GnRH abolished staining in both axons and perikarya, whereas preabsorption with
thyrotropin-releasing hormone
,
oxytocin
, arginine-vasopressin, and adrenocorticotrophic hormone did not affect staining intensity.
...
PMID:Immunohistochemical localization of gonadotropin-releasing hormone (GnRH) in the brain and infundibulum of the sheep. 701 81
JTP-4819 ((S)-2-[[(S)-2-(hydroxyacetyl)-1-pyrrolidinyl]carbonyl]-N- phenylmethyl)-1-pyrrolidinecarboxamide) is a potent (IC50: 0.83 +/- 0.09 nM in rat brain supernatant; 5.43 +/- 0.81 nM in Flavobacterium meningosepticum) and specific inhibitor of prolyl endopeptidase (PEP). JTP-4819 (3 mg/kg p.o.) exhibited a strong and durable ex vivo inhibitory effect on PEP in various regions of the rat brain. In addition, JTP-4819 inhibited the degradation of substance P, arginine-vasopressin,
thyrotropin-releasing hormone
, neurotensin,
oxytocin
, bradykinin, and angiotensin II by purified PEP with IC50 values of 9.6, 13.9, 10.7, 14.0, 4.5, 7.6 and 10.6 nM, respectively. In the one-trial passive avoidance test in rats with scopolamine-induced amnesia, JTP-4819 significantly prolonged the retention time when administered orally at doses of 1 and 3 mg/kg 1 hr before acquisition or at 3 and 10 mg/kg 1 hr before retention. In addition, coadministration of JTP-4819 and substance P, arginine-vasopressin or
thyrotropin-releasing hormone
(at doses at which each drug alone did not prolong the retention time) improved the retention time of rats with scopolamine-induced amnesia. Microdialysis studies demonstrated that JTP-4819 caused a significant increase in ACh release in the frontal cortex and hippocampus of young rats at oral doses of 1 and 3 mg/kg, as well as in both brain regions of aged rats at a dose of 3 mg/kg. These results indicate that JTP-4819 potentiates neuropeptide functions inhibiting PEP, that it activates cholinergic transmission and that it enhances learning and memory.
...
PMID:JTP-4819: a novel prolyl endopeptidase inhibitor with potential as a cognitive enhancer. 756 10
Rats drinking ad libitum tap water or hypertonic (i.e. 2%) sodium chloride solution were given intracerebroventricularly (i.c.v.), for three days,
thyrotropin-releasing hormone
(
TRH
) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride. Treatment with
TRH
resulted in significantly decreased hypothalamic
oxytocin
content in both euhydrated (i.e. given tap water ad libitum) and salt-loaded rats. In rats drinking tap water, neurohypophysial
oxytocin
content decreased. Plasma
oxytocin
concentration was distinctly elevated under
TRH
treatment in rats euhydrated but, on the contrary, decreased in salt-loaded rats as compared with animals similarly drinking hypertonic saline but not
TRH
-treated. The present data suggest that
TRH
may be involved in some regulatory processes related to
oxytocin
biosynthesis and release from the rat hypothalamo-neurohypophysial system.
...
PMID:Thyrotropin-releasing hormone (TRH) modifies oxytocin release from the hypothalamo-neurohypophysial system in salt-loaded rats. 767 Jan 25
Thyrotropin-releasing hormone,
oxytocin
, neurotensin, calcitonin gene-related peptide and neuropeptide Y have been proposed as putative neurotransmitters in the rostral ventrolateral medulla of the rat. To investigate the modulation of the basal blood pressure by neuropeptides, we microinjected these neuropeptides into the rostral ventrolateral medulla of the rat and examined their effects on basal blood pressure. Male Wistar rats were anesthetized with urethane, paralyzed and artificially ventilated. Thyrotropin-releasing hormone (0.01-1 ng),
oxytocin
(1 and 10 ng), neurotensin (0.1-10 ng), calcitonin gene-related peptide (1 and 10 ng) and neuropeptide (1 and 10 ng) produced increases in blood pressure and/or heart rate. Ganglion blockade with hexamethonium (10 mg/kg, i.v.) blocked the pressor responses to
thyrotropin-releasing hormone
(0.1 ng),
oxytocin
(10 ng) and neurotensin (10 ng), while methylatropine (1 mg/kg, i.v.) did not affect these responses. Corticotropin-releasing factor (0.1-10 ng) and atrial natriuretic peptide (1 and 10 ng) were ineffective. These findings indicate that many neuropeptides can modify basal blood pressure when injected into the rostral ventrolateral medulla. Whether these neuropeptides play a role in the blood pressure regulation within this brain region remains to be established.
...
PMID:Cardiovascular effects of microinjections of thyrotropin-releasing hormone, oxytocin and other neuropeptides into the rostral ventrolateral medulla of the rat. 821 15
Rats euhydrated and dehydrated during two or four days were given intracerebroventricularly (i.c.v.)
thyrotropin-releasing hormone
(
TRH
) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride. A single dose of
TRH
injected to euhydrated animals increased the hypothalamic vasopressin content but did not affect significantly the content of vasopressin in the neurohypophysis as well as that of
oxytocin
both in the hypothalamus and neurohypophysis. In rats deprived of water for two days
TRH
completely prevented the decrease of neurohypophysial
oxytocin
due to stimulation of osmoreceptor origin. Similarly,
TRH
restrained both the hypothalamic and the neurohypophysial vasopressin and
oxytocin
depletion in rats dehydrated for four days.
...
PMID:Thyrotropin-releasing hormone (TRH) modulates vasopressin and oxytocin release from the hypothalamo-neurohypophysial system in dehydrated rats. 824 30
Rats drinking and libitum tap water or hypertonic (i.e., 2%) sodium chloride solution were given intracerebroventricularly (i.c.v.), during three days,
thyrotropin-releasing hormone
(
TRH
) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride. Treatment with
TRH
resulted in significantly increased hypothalamic
oxytocin
content in both euhydrated (i.e., given tap water ad libitum) and salt-loaded rats and vasopressin content only in euhydrated rats. Similarly, neurohypophysial vasopressin and
oxytocin
content significantly increased in animals drinking tap water or 2% sodium chloride during treatment with
TRH
. The present data suggest that
TRH
may be involved in some regulatory processes to vasopressin and
oxytocin
biosynthesis and release from the rat hypothalamo-neurohypophysial system.
...
PMID:Influence of thyroliberin (TRH) on hypothalamo-neurohypophysial vasopressin and oxytocin content of rats drinking 2% NaCl. 830 34
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