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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The neurohypophysial hormones oxytocin and arginine vasopressin (AVP) have been identified on immunological criteria in the ovary. Confirmation of extraneuronal synthesis requires the demonstration in the tissue of the specific messenger RNA (mRNA) for the preprohormone. Using a synthetic pentadecamer nucleotide probe, highly specific for the 5' region of rat neurophysin II (NP II), we have demonstrated the presence of AVP-NP II mRNA in the ovary of Sprague-Dawley, Long-Evans and Brattleboro rats, with an apparent molecular weight identical to that seen for hypothalamus. These findings, together with the presence of immunoreactive AVP in the ovaries but not hypothalami of Brattleboro rats, suggest that tissue-specific differences in AVP-NP II gene expression occur at the translational as well as transcriptional level.
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PMID:Vasopressin-neurophysin II gene expression in the ovary: studies in Sprague-Dawley, Long-Evans and Brattleboro rats. 399 49

The very potent opioid peptide, dynorphin, has recently been shown by radioimmunoassay and immunocytochemical techniques to be selectively concentrated in the pars nervosa of pituitary, suggesting a possible association of dynorphin with the neurohypophyseal hormones, vasopressin and oxytocin. In this study, we report that pituitary and brain contents of immunoreactive dynorphin in homozygote Brattleboro rats (unable to synthesize vasopressin) are similar to those in heterozygote animals and in normal Long-Evans rats. Thus, the syntheses of immunoreactive dynorphin and vasopressin in the hypothalamo-hypophyseal tract appear to be independently regulated.
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PMID:Levels of immunoreactive dynorphin in brain and pituitary of Brattleboro rats. 613 55

Brattleboro rats exhibit diabetes insipidus (DI) because of a genetic autosomal recessive defect in the synthesis of vasopressin; oxytocin is synthesized normally. Preliminary work suggests that elevated circulating oxytocin levels may compensate for the absence of vasopressin. To evaluate the consequences of presumed elevations of oxytocin levels, oxytocin binding and tissue responsiveness have been measured in the uterus and epididymal fat cells of homozygous-DI (HoDI) and heterozygous-DI (HeDI) animals and Sprague-Dawley and Long-Evans controls. Surprisingly, whereas membranes from HoDI rat uteri exhibited an 85% reduction in oxytocin binding, the biological response (contraction) to oxytocin was indistinguishable from the uteri of HeDI or Sprague-Dawley animals. The uterine response to carbachol was also normal in HoDI rats. In contrast, in adipocytes from HoDI animals, the biological response to oxytocin (glucose oxidation) was abolished, whereas the binding of oxytocin was normal; insulin-stimulated glucose oxidation was, however, normal. These results indicate that receptor binding, while critical to hormone action, is not the sole determining factor. With oxytocin action, postreceptor mechanisms are most important in determining oxytocin responsiveness.
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PMID:Oxytocin action: lack of correlation between receptor number and tissue responsiveness. 626 73

Rat pituitary neural lobe contained high concentrations of cholecystokinin-like immunoreactivity (CCK-LI). Section of the pituitary stalk resulted in loss of CCK-LI, and both lactation and replacement of drinking water with 2% saline resulted in marked depletion of CCK-LI. Rats with congenital diabetes insipidus (Brattleboro strain) had a 73% reduction in CCK-LI below the levels of hooded Long-Evans controls, where as levels in the brain were unchanged. Release of CCK-LI, labeled dopamine, and gamma-amino butyric acid in response to potassium depolarization was studied. There was a low fractional release of CCK-LI. Addition of sulfated CCK-8 (CCK-8s) to the medium enhanced the calcium-dependent potassium-stimulated release of dopamine, but basal release was unaffected. gamma-Amino butyric acid release was only poorly calcium dependent and not effected by extracellular CCK-8s. Vasopressin and oxytocin release were stimulated by electrical stimulation of the pituitary stalk, and were unaffected by the addition of CCK-8s to the medium. In vivo, however, the injection of 5 micrograms CCK-8s into the third ventricle resulted in increased plasma vasopressin concentrations.
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PMID:Localization and actions of cholecystokinin in the rat pituitary neurointermediate lobe. 632 36

This investigation has confronted some very basic questions of neurobiology and specifically deals with the neurovascular and neuroanatomical interactions that occur between graft and host following neural transplantation. Host Long-Evans rats with chronic autosomal diabetes insipidus (DI) received stereotaxic implants of normal 17 day post-coitus fetal hypothalamic fragments from the rostral (anterior) hypothalamus of normal Long-Evans pups. Following stereotaxic surgery DI hosts were killed 60 or 90 days later and their brain prepared for correlative microangiography-immunocytochemistry coupled with transmission electron microscopy. Explants were rapidly invaded by host vessels from several routes. (1) Vessels appeared to arise from portal capillaries in the underlying median eminence and (2) from adjacent vessels from the paraventricular nucleus and surrounding endocrine hypothalamus and (3) possibly from intrinsic vessels of the graft. The former remained fenestrated and established bonafide neurovascular zones in the ventral regions and in actively growing explants. Small clusters of arginine vasopressin-positive fibers and neurophysin positive neurons were noted throughout the parenchyma of explants. Despite the presence of neurosecretory neurons and neurovascular (neurohemal) zones, none of the host rats exhibited a physiological return to normal parameters of water balance. However the active growth and development of explants in the third cerebral ventricle of DI host rats coupled with emergence of neurovascular zones lends support to a potential model for analyzing the development of anatomical substrates for the central delivery of neuropeptide hormones.
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PMID:Neuronal and neurovascular integration following transplantation of the fetal hypothalamus into the third cerebral ventricle of adult Brattleboro rats. Neurological transplants: I. 633 69

Comparative ultrastructural localization of corticotropin-releasing factor (CRF) and oxytocin was performed in the rat median eminence of Long Evans and Brattleboro rats. The peroxidase-antiperoxidase technique used on serial ultrathin sections revealed CRF and oxytocin neurosecretory granule colocalization in the same fibers of the internal layer running towards the posterior pituitary. It is probable that both these peptides coexist in the same granules. In the Brattleboro rats, while genetically lacking vasopressin, CRF was nevertheless shown to be present. In these rats, as was demonstrated in the Long Evans rats, CRF distribution paralleled that of oxytocin only in the internal zone of the median eminence.
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PMID:Comparative immunoelectron microscopic localization of corticotropin-releasing factor (CRF-41) and oxytocin in the rat median eminence. 633 45

We have evaluated factors, other than genetic, which might be related to the lack of an oxytocin-mediated insulinlike response (glucose oxidation; lipogenesis) in adipocytes from Brattleboro rats, homozygous for the diabetes insipidus trait (HoDI rats). The manoeuvres used in an attempt to restore the glucoregulatory responses to oxytocin in HoDI cells (increased glucose in the fat pad digestion medium; increased calcium concentration in the oxidation assay; estrogen treatment; use of [1-14C]glucose as substrate; inclusion of adenosine in the assay medium; vasopressin replacement therapy) uniformly failed to result in oxytocin activation of HoDI adipocytes. In contrast, the contractile responses of estrogenized HoDI rat uteri were indistinguishable from those of estrogenized normal rats. We conclude that the nonresponsiveness of the Brattleboro adipocytes to the glucoregulatory actions of oxytocin is not due to factors related to the conditions of the bioassay. On the other hand, in normal fat cells (from Sprague-Dawley and Long Evans rats), oxytocin responsiveness was augmented by a number of the manoeuvres mentioned above, most notably by the inclusion of either calcium (10 mM) or adenosine (10 microM) in the assay medium. Nonetheless, the maximum oxytocin responsiveness of adipocytes from Long Evans or Sprague-Dawley rats, under all conditions of assay, was still only a fraction (less than 20%) of the maximal response to insulin. The effect of adenosine on oxytocin action (increased sensitivity, without an effect on the maximum response) is in keeping with the previously observed effects of this nucleoside on the action of insulin; our results thus pointed to a new parallel in the action of insulin and oxytocin.
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PMID:Oxytocin resistance in Brattleboro rat adipocytes and comparative studies on insulin or oxytocin responsiveness in normal rat adipocytes. 636 6

Brattleboro (diabetes insipidus) rats showed a delayed recovery from 6-hydroxydopamine (6-OHDA) hypotension as compared to Long Evans controls. A slight increase in circulating arginine vasopressin was noted in the 6-OHDA-treated Long Evans rats but no change in circulating oxytocin was apparent in either species. The haematocrit and plasma potassium suggested haemodilution in Long Evans rats following 6-OHDA treatment but no such changes were apparent in similarly treated Brattleboro rats. Since the major difference in Long Evans and Brattleboro rats is the latter's inability to synthesize arginine vasopressin (AVP), it is suggested that AVP may have a role in the restoration of homeostasis following 6-OHDA-induced hypotension. This conclusion is supported by (a) a delayed recovery from hypotension and (b) no change in blood concentration parameters, in the Brattleboro rat.
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PMID:Reversal of 6-hydroxydopamine-induced hypotension in Long Evans and diabetes insipidus (Brattleboro) rats. 640 2

The present paper reviews recent work conducted in our laboratory on vasopressin neurons either grown in culture or transplanted into vasopressin deficient rats. The in vitro model of reaggregated cell culture used the anterior hypothalamus, including vasopressin neurons of the SON from normal timed-pregnant LE rats of similar ages used in our in vivo model. Various cells were co-cultured with their known target tissue, the posterior pituitary to analyze further the influence of the target tissue on hormone production. At a designated end point, cultured cells were fixed and stained immunocytochemically for vasopressin and neurophysin. Radioimmunoassay of the samples was performed for vasopressin quantification. Hypothalamic cells from all ages produced vasopressin (VP). The co-culturing of hypothalamus with posterior pituitary produced a significant increase in VP. Correlative transplantation studies were conducted using timed-pregnant Long-Evans (LE) rats at various days post coitus (dpc) and neonatal tissue from 0- and 5-day old rat pups. Animals survived about 40 days then were perfused and their brains processed for vasopressin and neurophysin thick-section immunocytochemistry. The results showed that the capability for survival of younger grafts was much greater than that of older tissue. With this paper, we have shown that the reaggregation of anterior hypothalamic cells in a culture system can be used for microassay of neurosecretory activity. These data suggest a close correlation between the ability of a neuron to survive transplantation and its stage of development. With the present studies, we have shown that neurons not fully differentiated maintain a greater degree of plasticity than older tissue and are better able to survive the rigors of transplantation and that various manipulations of environmental factors have an effect on brain development at critical times.
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PMID:In vitro and in vivo studies on development and regeneration of vasopressin neurons. 648 53

An indirect immunofluorescence technique was used to study the peptidergic innervation of the thyroid gland in homozygous Brattleboro rats (DI) and normal Long-Evans rats (LE). The primary goal of this study was to determine whether the previously demonstrated decrease in thyroid responsiveness to TSH in DI might be due to an abnormality in the innervation of the thyroid. Thyroids from both types of rats were found to contain nerve fibers containing immunoreactivity for vasoactive intestinal peptide (VIP), substance P (SP), neuropeptide Y (NPY), and peptide HI (PHI). All four types of fibers were found in close association with both follicle cells and blood vessels. Well developed networks of fibers surrounding blood vessels were particularly apparent in the case of NPY. The density of fibers associated with follicle cells in DI was at least as great as that in LE in regard to SP, NPY, and PHI. Fibers containing VIP were found in greater abundance in DI than in LE. Additional studies revealed no evidence of thyroid fibers containing either somatostatin or neurophysin, which was used as a marker for vasopressin. We conclude that the reduced responsiveness of the thyroid in DI is not due to an inadequate supply of any of the neuropeptides included in this study. Since VIP is known to enhance thyroid secretion, we suggest that the apparent proliferation of VIP-containing fibers in DI may be a reflection of a neural mechanism attempting to compensate for a thyroid gland deficiency analogous to the humoral mechanism by which TSH secretion increases in response to thyroid deficiency.
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PMID:Immunocytochemical studies of the peptidergic innervation of the thyroid gland in the Brattleboro rat. 654 94


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