Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous immunocytochemical studies reported that when specific monoclonal antibody directed against vasopressin (VP) (VP-MAb) was injected in vivo above the rat hypothalamic nuclei, it penetrated and was specifically transported by VP-producing neurons. In this study, using the same methodological approach, the fate of monoclonal antibody directed against corticotropin-releasing factor (CRF) (CRF-MAb) injected in vivo above the paraventricular nucleus (PVN) of the rat brain was investigated by immunocytochemistry in male Zucker rats and adrenalectomized or colchicine-pretreated male Long-Evans rats. The simultaneous immunocytochemical localization of the injected CRF-MAb and endogenous peptides and enzyme synthesized by the neurons penetrated by the antibody, demonstrated that CRF-MAb was mainly detected in CRF neurons. But the CRF-MAb was also detected in VP, oxytocin, neuropeptide Y and tyrosine hydroxylase-producing neurons of the PVN. CRF-MAb was therefore localized in PVN neurons which synthesize CRF and in PVN neurons with physiological and morphological relationships with the CRF peptidergic system. Before obtaining biological effects of injected CRF-MAb, the results described here suggest that specific monoclonal antibodies provide a useful specific tool for elucidating the functional relationships between neuronal systems.
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PMID:Uptake of a monoclonal antibody to corticotropin-releasing factor (CRF) into rat hypothalamic neurons. 237 97

Pantethine, a cysteamine precursor, depletes somatostatin in the cerebral cortex and hypothalamus and prolactin in the anterior pituitary and hypothalamus. This study investigated the effect of pantethine on oxytocin and arginine vasopressin content in the posterior pituitary and hypothalamus. Male Long-Evans rats were injected intraperitoneally with escalating doses of pantethine (i.e., 146.7 mg, 293.4 mg and 586.6 mg/100 gm body weight). Hormone content was determined by radioimmunoassay. Three hours after pantethine treatment, the oxytocin content in the posterior pituitary and the hypothalamus was markedly reduced with all doses of the drug. Vasopressin content in the posterior pituitary and hypothalamus was decreased but to a lesser extent than oxytocin and only with the highest dose of pantethine. Pantethine may act to reduce oxytocin and vasopressin content through intracellular conversion to cysteamine. The exact mechanism of action of pantethine on oxytocin and vasopressin remains to be elucidated.
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PMID:Changes in oxytocin and vasopressin content in posterior pituitary and hypothalamus following pantethine treatment. 240 77

A comparative quantitative analysis was carried out on identified supraoptic neurones of male and female Wistar and Long Evans rats under normal conditions and after chronic osmotic stimulation, and in homozygous Brattleboro rats suffering from diabetes insipidus. The neurones were identified by immunocytochemical or morphological means. Osmotic stimulation resulted in significant increases in the number and extent of direct neuronal appositions and in the number of presynaptic terminals contacting two neurosecretory cells simultaneously ("double" synapses). In the supraoptic nuclei of both sexes these increases were restricted to the oxytocin secreting neurones. In Brattleboro homozygous rats treated with vasopressin, the proportion of oxytocinergic neurones in apposition was not modified, but the number of appositions per soma profile decreased as did the incidence of "double" synapses. In nuclei of osmotically stimulated rats, increase in cell volume affected both types of neurosecretory cell and was accompanied by an increase of the absolute extent of glial coverage. However, the extent of glial coverage of the oxytocinergic neurones did not match the hypertrophy of the cells, resulting in a decrease in their relative glial coverage, compared to normal hydrated animals. The increased neuronal appositions, therefore, cannot result simply from a retraction of glial processes. The structural reorganization of the oxytocinergic system observed during chronic osmotic stimulation was as extensive as that observed at lactation. Moreover, the changes were as extensive in Wistar as in Brattleboro lactating rats, although the latter have an added osmotic stimulus. This implies that lactation and osmotic stimulation do not produce additive effects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Osmotic stimulation causes structural plasticity of neurone-glia relationships of the oxytocin but not vasopressin secreting neurones in the hypothalamic supraoptic nucleus. 242 93

Fetal hypothalami obtained from normal Long-Evans rats were transplanted to the lateral, third or fourth ventricle of adult male Brattleboro rats, homozygous for diabetes insipidus. The density of the capillary plexuses within the grafts did not vary as a function of their intraventricular location; all transplants exhibited a capillary density equivalent to that of the in situ hypothalamus. Intravascular injections of HRP resulted in retrograde neuronal labeling only in grafts that were attached to circumventricular organs of the host brain, especially the median eminence. Typically, HRP-associated label was confined to vascular and perivascular elements and not diffusely distributed within the graft parenchyma, indicating that capillaries within the transplants developed barrier properties similar to those of the native hypothalamus. Neural integration of the transplant with the recipient brain was limited; at most points of apposition the neuropil of graft and host were separated by an intervening ependymal layer or glia limitans. All surviving grafts contained neurophysin and/or vasopressin-immunoreactive (VP-ir) neurons. Three anatomically distinct populations of VP-ir neurons were identified. Magnocellular VP-ir neurons were identified in less than half of the grafts, and when present they were few in number distinct, but sparse vasopressinergic innervation of median eminence capillaries was observed in all cases where grafts containing magnocellular neurons were apposed to this structure. Most grafts contained numerous, parvicellular VP-ir neurons arranged in aggregations which resembled the suprachiasmatic nucleus (SCN). SCN-like cell groups projected to neural targets within the graft and the host brain, but they did not project onto blood vessels. A second, distinct class of parvicellular VP-ir neuron also was identified in a majority of transplants. In contrast to SCN-like ('type' I) cells, these 'type II' parvicellular neurons were somewhat larger and found in less discretely organized groups, and they projected to vascular targets; usually locally elaborated capillary plexuses intrinsic to the transplants. In the present study, there was no amelioration of the symptoms of diabetes insipidus in the host animals despite the presence of numerous VP-ir neurons in virtually all grafts. This was probably related to the limited survival of magnocellular VP-ir neurons, which appear to be the principal source of vasopressinergic projections from the graft to fenestrated capillary plexuses of the host brain.
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PMID:Characteristics of vasculature and neurovascular relations in intraventricular anterior hypothalamic transplants. 244 72

The effects of arginine vasopressin (AVP), and of the V2-AVP receptor agonist 1-deamino[8-D-arginine] vasopressin (DDAVP) on release from the vasopressin-neurons and oxytocin-neurons of Long-Evans rats were evaluated using specific radioimmunoassays for rat neurophysins. AVP (1 microgram, 1 nmol) or DDAVP (25 ng, 25 pmol) was administered i.p. to animals 1 h before they received an i.v. infusion of 18% saline at 10 microliters/100 g b. wt./min for 60 min. Both AVP and DDAVP decreased the responsiveness (slope) but not the sensitivity threshold of vasopressin-neurons to acute changes in plasma osmolality. Since the amounts of the peptides giving comparable decreases in responsiveness were directly related to their antidiuretic potencies, it is most probable that this influence is mediated through V2-like receptors. However, while ruling out a significant contribution of V1-type receptors, the data do not exclude involvement of other vasopressin receptors (e.g. V3-type receptors). Both AVP and DDAVP also appeared to have an inhibitory effect on release from oxytocin-neurons, but in this case they significantly altered sensitivity threshold but not responsiveness to acute changes in plasma osmolality. Because AVP produced a shift in sensitivity threshold larger than that by DDAVP when the peptides were used in amounts related to their antidiuretic potencies, our results suggest that the feedback influence of AVP on oxytocin-neurons is largely, although not entirely, exercised through V2-like receptors.
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PMID:Vasopressin reduces release from vasopressin-neurons and oxytocin-neurons by acting on V2-like receptors. 252 39

1. The effects of mu- and K-opiate receptor agonists on plasma concentrations of immunoreactive (ir) oxytocin (OXY) and arginine vasopressin (AVP) in normally hydrated and water-deprived rats were studied. 2. Water-deprivation for 36 h elevated both plasma ir-OXY and ir-AVP concentrations of Long-Evans rats. These elevated levels were lowered in a dose-dependent manner after subcutaneous administration of bremazocine (3-10 micrograms/kg), M320 (10-100 micrograms/kg) or morphine (0.1-10 mg/kg). Comparable reductions of plasma concentrations of ir-AVP and ir-OXY were observed. 3. Plasma concentrations of ir-OXY and ir-AVP of normally hydrated Long-Evans rats were lower after subcutaneous administration of bremazocine (10 micrograms/kg), M320 (10 micrograms/kg) and morphine (1.0 mg/kg). 4. These data suggest that both mu- and K-opiate receptor agonists inhibit both OXY and AVP release from the neurohypophysis of rats.
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PMID:mu- and K-opiate receptor agonists reduce plasma neurohypophysial hormone concentrations in water-deprived and normally hydrated rats. 254 54

1. This study utilized retrograde anatomical tracer techniques and in vivo extracellular electrophysiological studies to examine caudal ventrolateral and dorsomedial medulla afferents to supraoptic nucleus neurosecretory neurones in male Long-Evans rats. 2. In one series of experiments, pentobarbitone-anaesthetized animals were subjected to ventral exposure of the hypothalamus and rhodamine-tagged latex microspheres (0.05-0.2 microliter) were injected into one supraoptic nucleus. Following perfusion with paraformaldehyde-glutaraldehyde 18-24 h later, cell counts were obtained of rhodamine- and/or catecholamine-labelled neurones in the caudal ventrolateral and dorsomedial medulla both ipsi- and contralateral to the injection site. 3. In the caudal ventrolateral medulla, each injection labelled fewer than 15% of the catecholaminergic neurones; with small injections, most (68-100%) of the rhodamine-labelled neurones also displayed catecholamine histofluorescence. In the caudal nucleus tractus solitarii, one-half to one-third as many rhodamine-labelled cells were observed, but a higher percentage (13-100%) of these were non-catecholaminergic. 4. Extracellular recordings were obtained from antidromically identified supraoptic neurones classified as vasopressin (n = 106) or oxytocin (n = 26) secreting. Single cathodal pulses (0.2 ms duration, 0.02-0.08 mA) applied in the caudal half of the ipsilateral nucleus tractus solitarii evoked a transient (30-50 ms) activation of 63% of both vasopressin- and oxytocin-secreting neurones. Mean latencies (+/- S.E.M.) for vasopressin and oxytocin cells were 49.8 +/- 1.0 and 46.5 +/- 2.4 ms respectively; these were not significantly different. Similar responses were noted to contralateral stimuli applied to four vasopressin and two oxytocin cells. 5. Vasopressin neurones activated by caudal nucleus tractus solitarii stimulation displayed similar patterns of response to stimulation in the caudal ventrolateral medulla. However, latencies from the nucleus solitarius (mean 47.6 +/- 1.4 ms; n = 59) were significantly longer (P less than 0.05) than from the ventrolateral medulla (41.5 +/- 2.0 ms; n = 17). In eight out of eleven vasopressin neurones tested, interruption of synaptic transmission through the ventrolateral medulla reduced or abolished the caudal nucleus tractus solitarii-evoked excitation but had no effect on their response to baroreceptor activation. This manoeuvre affected zero out of five oxytocin cells similarly excited by nucleus solitarius stimulation. 6. These observations indicate that visceral input mediated through the nucleus tractus solitarii is transmitted differentially to supraoptic vasopressin- and oxytocin-secreting neurones.
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PMID:Dorsomedial medulla stimulation activates rat supraoptic oxytocin and vasopressin neurones through different pathways. 262 94

This study investigated the mechanisms by which fetal hypothalamic transplants promote functional recovery in neurohypophysectomized rats. Seven days after neurohypophysectomy (resulting in urine osmolalities of about 800 mOsm), young adult male Long-Evans rats received either fetal hypothalamic grafts (n = 10) or sham transplants (n = 7). Recovery from the lesioned-induced diabetes insipidus was monitored for 6 months and then the transplant sites were evaluated by immunocytochemistry. Surviving host supraoptic magnocellular neurons and neurophysin-positive grafted neurons were counted and their formation of neurohemal contacts evaluated by retrograde transport of systemically injected horseradish peroxidase (HRP). There were significantly more surviving supraoptic magnocellular neurons in neurohypophysectomized animals with median eminence-placed grafts (2236 +/- 261 neurons/animal) than in animals with ectopic tissue grafts (895 +/- 142 neurons/animal) or sham implants (1052 +/- 92 neurons/animal). Almost all surviving host magnocellular neurons were labeled with retrogradely transported HRP while virtually none of the grafted neurophysin positive cells showed evidence of HRP uptake. The degree of functional recovery was directly correlated with the increased survival of host neurons. By 8 weeks post-transplantation, animals with median eminence-placed grafts had recovered from their diabetes insipidus and could concentrate their urine to within normal limits (2,120 +/- 110 mOsm). This recovery was stable for the remainder of the 6 month test period. In contrast, animals with ectopic grafts and sham transplants had permanent deficits in fluid regulation. Our results provide evidence for the long-term capacity of fetal neural tissue implants to rescue host neurons from the cell death that typically occurs in the mature central nervous system after axotomy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fetal hypothalamic transplants promote survival and functional regeneration of axotomized adult supraoptic magnocellular neurons. 270 2

The role of central nervous system arginine vasopressin (AVP) and oxytocin (OXY) in the cardiovascular response to acute stress was examined using three experimental models: pharmacological antagonism of central AVP-OXY receptors; lesions of the paraventricular nucleus (PVN); and rats genetically lacking in AVP synthesis, i.e., the Brattleboro strain. Central administration of an AVP-OXY antagonist abolished the increase in heart rate (HR) seen following acute footshock stress. The group receiving centrally administered antagonist increased HR 15 +/- 17 (SE) beats/min, whereas, in contrast, the group receiving intravenous administration of the antagonist showed a 66 +/- 17 beats/min increase, and the group receiving intraventricular antagonist vehicle showed a 101 +/- 14 beats/min increase in response to stress. In a second study, electrolytic lesions of the PVN also blocked the increase in HR seen following stress, 20 +/- 12 beats/min for PVN-lesioned rats, 74 +/- 25 beats/min for sham lesion rats, and 93 +/- 7 beats/min for rats with a lesion not destroying the PVN. In the final study, the responses of Brattleboro rats, i.e., rats genetically deficient in vasopressin synthesis, were equivalent to their Long-Evans controls (131 +/- 13 and 147 +/- 12 beats/min, respectively). In each of these studies, the blood pressure responses to the stressor were equivalent for control and experimental groups. The results of these studies suggest that a neuropeptide system originating in or passing through the PVN may play an important role in the cardiovascular responses to stress and further suggest that the central OXY system may be one pathway mediating this response.
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PMID:Central oxytocin systems may mediate a cardiovascular response to acute stress in rats. 271 34

Acetylcholinesterase activity was demonstrated histochemically at light- and electron-microscopic levels, in Vibratome sections of the supraoptic nucleus of fixed hypothalami derived from osmotically stimulated and unstimulated Long Evans rats, from homozygous Brattleboro rats with hypothalamic diabetes insipidus, from lactating rats, from normal adult male house mice (Mus musculus) and from mice with hereditary nephrogenic diabetes insipidus (di/di). Reaction product was located in supraoptic magnocellular neurons; in dorsal and rostral aspects of the supraoptic nuclei lightly stained cells predominate, whereas in ventral and caudal regions densely staining perikarya predominate. Pre- and post-embedding immunocytochemical detection of oxytocin-neurophysin or vasopressin-neurophysin, combined with acetylcholinesterase histochemistry, showed that the lightly staining cells are oxytocinergic, and the densely staining cells vasopressinergic. Osmotic stimulation of the animals, either by substitution of drinking water for 3 days with 2.5% saline or reason of genetic defects which result in diabetes insipidus, enhanced the acetylcholinesterase activity of the vasopressin neurons but had little effect on the weekly acetylcholinesterase-reactive oxytocin cells. Acetylcholinesterase activity was particularly marked in the hypertrophied abnormal magnocellular neurons of homozygous Brattleboro rats which do not release significant amounts of vasopressin. The increased acetylcholinesterase activity in osmotically stimulated animals cannot, therefore, be a function of vasopressin. Acetylcholinesterase activity was also detected in large multipolar neurons lying dorsolateral to the supraoptic nucleus, and in their fine axonal processes which project towards the supraoptic nucleus. A very few synaptic boutons surrounded by acetylcholinesterase reaction product were found in contact with magnocellular neuron basal dendrites. However, much of the punctate acetylcholinesterase reactivity observed at the light microscopic level and previously interpreted as representing the loci of cholinergic synaptic boutons was shown to be intracellular, and probably caused by acetylcholinesterase activity in some large, secondary lysosomes.
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PMID:Differential distribution of acetylcholinesterase activity among vasopressin- and oxytocin-containing supraoptic magnocellular neurons. 276 86


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