Intracellular Ca(2+) channel immunoreactivity in neuroendocrine axon terminals.
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The concentration of neuroendocrine terminals in the neurohypophysis facilitates the identification and localization of Ca(2+) channel subtypes near neuroendocrine release sites. Immunoblots of rat neurohypophysial tissue identified the alpha(1)1.3, alpha(1)2.1, alpha(1)2.2, and alpha(1)2.3 Ca(2+) channel subunits. Immunofluorescence staining of axon terminal plasma membranes was weak, suggesting that Ca(2+) channels are dispersed. This contrasts with the highly punctate alpha(1)2.2 immunoreactivity in bovine chromaffin cells; the neurohypophysial terminals may therefore lack the specialized release zones found in those cells. Immunofluorescence and immunogold labeling identify dense core granule-like structures in the terminal cytoplasm containing multiple Ca(2+) channel types. Ca(2+) channels in internal membranes may play an important role in channel targeting and distribution in neuroendocrine cells. (+info)
Neurohypophysial hormone receptors and second messengers in trout hepatocytes.
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Neurohypophysial hormone receptors and second messengers were studied in trout (Oncorhynchus mykiss) hepatocytes. Arginine vasotocin (AVT) and isotocin (IT) elicited a concentration-dependent inhibition of cAMP accumulation in the presence of 5x10(-8) M glucagon (maximal effect for 4.5x10(-7) M and 1.4x10(-7) M, half-maximal effect for 2.1x10(-8) M and 0.7x10(-8) M, AVT and IT respectively). The effect of glucagon was inhibited up to 90% by AVT and 80% by IT. While AVT inhibited (up to 50%) the basal cAMP production, IT had no such action. Specific V(1) or V(2) analogues (with reference to vasopressin in mammals) were used for pharmacological characterization of the type of neurohypophysial hormone receptor involved in this inhibition. The V(1) agonist [Phe(2), Orn(8)]-oxytocin inhibited the glucagon-stimulated cAMP production with a maximal effect for 6x10(-7) M and a half-maximal effect for 0.9x10(-8) M concentrations of the analogue. While the V(1) agonist reduced the glucagon-stimulated cAMP level by 70%, it showed only a tendency to reduce the basal level. The V(2) agonist [deamino(1), Val(4),d -Arg(8)]-vasopressin had no effect either on basal or on glucagon-stimulated cAMP production. The V(1) antagonist [d(CH(2))(5)(1), O-Me-Tyr(2), Arg(8)]-vasopressin totally reversed the 10(-8) M AVT-induced inhibition of 5x10(-8) M glucagon-stimulated cAMP production, whereas the V(2) antagonist [d(CH(2))(5)(1),d -Ile(2), Ile(4), Arg(8), Ala(9)]-vasopressin had no such effect. In this particular case, maximal and half-maximal effects of the V(1) antagonist were obtained for 2.3x10(-6) M and 1. 2x10(-6 )M respectively. Changes in intracellular calcium content were measured using the fluorescent probe FURA-2/AM. AVT and IT elicited a concentration-dependent increase in Ca(2+) accumulation. The comparison of the effect of 10(-8) M agonists versus AVT showed the following order of potency: AVT=IT>V(1) agonist>V(2) agonist. The V(1) antagonist reversed the AVT-induced Ca(2+) accumulation whereas the V(2) antagonist had no such effect. These results are taken as evidence for the presence in trout hepatocytes of neurohypophysial hormone receptors functionally close to the V(1a)-type linked to cAMP production and Ca(2+) mobilization. (+info)
The murine Otp homeobox gene plays an essential role in the specification of neuronal cell lineages in the developing hypothalamus.
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Hypothalamic nuclei, including the anterior periventricular (aPV), paraventricular (PVN), and supraoptic (SON) nuclei strongly express the homeobox gene Orthopedia (Otp) during embryogenesis. Targeted inactivation of Otp in the mouse results in the loss of these nuclei in the homozygous null neonates. The Otp null hypothalamus fails to secrete neuropeptides somatostatin, arginine vasopressin, oxytocin, corticotropin-releasing hormone, and thyrotropin-releasing hormone in an appropriate spatial and temporal fashion, and leads to the death of Otp null pups shortly after birth. Failure to produce these neuropeptide hormones is evident prior to E15.5, indicating a failure in terminal differentiation of the aPV/PVN/SON neurons. Absence of elevated apoptotic activity, but reduced cell proliferation together with the ectopic activation of Six3 expression in the presumptive PVN, indicates a critical role for Otp in terminal differentiation and maturation of these neuroendocrine cell lineages. Otp employs distinct regulatory mechanisms to modulate the expression of specific molecular markers in the developing hypothalamus. At early embryonic stages, expression of Sim2 is immediately downregulated as a result of the absence of Otp, indicating a potential role for Otp as an upstream regulator of Sim2. In contrast, the regulation of Brn4 which is also expressed in the SON and PVN is independent of Otp function. Hence no strong evidence links Otp and Brn4 in the same regulatory pathway. The involvement of Otp and Sim1 in specifying specific hypothalamic neurosecretory cell lineages is shown to operate via distinct signaling pathways that partially overlap with Brn2. (+info)
Uptake of radiolabeled estradiol by the canine adrenal.
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Tritiated estradiol injected intravenously into 11 mongrel dogs sacrificed at 3, 7, 10, 17, and 60 min showed maximum uptake in the adrenal gland at 3-7 min. The concentrations of radioactivity in the adrenal in percent dose per gram equaled that from 131I-19-iodocholesterol. If a 131I-estradiol could be synthesized that would concentrate similarly in the adrenal, it would offer the advantage of almost instantaneous imaging after the tracer injection and a lower radiation dose. (+info)
Pituicytoma: primary astrocytic tumor of the pars nervosa in aging Fischer 344 rats.
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We describe 2 cases of a relatively rare tumor diagnosed as pituicytoma in the pars nervosa of rat pituitary. This tumor was spontaneously noted in one 110-week-old female and one 109-week-old male Fischer 344 (F344)/DuCrj rats during 2-year carcinogenicity studies. Although no gross abnormality of the pituitary was detected in the female rat, whitish discoloration and enlargement of the pituitary were observed in the male. Histopathologically, neoplastic cells in both animals possessed pale eosinophilic, often abundant irregular cytoplasm with nuclei of variable size. The tumor cells were arranged in the spindle or sheet cell pattern with indistinct cell boundaries and showed compression or invading proliferation of surrounding tissues. Prominent pleomorphism of the cells was noted in the tumor in the female rat, and mitotic figures were detected in several portions of the tumor in the male rat. Small-sized cells having scanty cytoplasm with deeply staining nuclei seen in the mass were suspected to be microglia. Moreover, isolated single native pars distalis cells were distributed throughout the tumor masses. Immunohistochemically, cytoplasmic foot process of the tumor cells showed a positive immunoreactivity for glial fibrillary acidic protein. On the basis of morphologic characteristics and glial fibrillary acidic protein staining, this tumor is consistent with astrocytoma. (+info)
Tyrosine hydroxylase in vasopressinergic axons of the pituitary posterior lobe of rats under salt-loading as a manifestation of neurochemical plasticity.
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In this study, we attempted to test whether tyrosine hydroxylase (TH), the first rate-limiting enzyme of catecholamine synthesis, is confined to the perikarya of activated magnocellular vasopressinergic (VPergic) neurons or is also present in their distal axons in the pituitary posterior lobe (PL). In addition, we evaluated the possible correlation between TH and VP turnover in the axons of rats drinking 2% NaCl for 1, 2, and 3 weeks. To this aim, we examined the large swellings of VPergic axons, the so-called Herring bodies, using the double-immunofluorescent technique and the avidinbiotin technique, combined with image analysis. Here we have demonstrated for the first time a colocalization of TH and VP in Herring bodies, which is a strong argument in favor of TH transport from the perikarya of VPergic neurons via axons toward their terminals. TH-immunoreactive (IR) and VP-IR materials were distributed in Herring bodies with seeming zonality. The number of VP-IR Herring bodies decreased by a factor of four over the first week of osmotic stimulation, remaining at almost the same low level until the end of the experiment. Conversely, the content of the VP-IR material within the individual Herring bodies fell gradually during the three weeks of salt-loading. The results suggest that VP depletion from Herring bodies prevails in its transport into these structures during the whole period of osmotic stimulation. In contrast to VP-IR Herring bodies, the number of TH-IR Herring bodies and the content of TH-IR material within the individual Herring bodies increased progressively during the entire experiment. The synchronization of the VP depletion and TH accumulation in Herring bodies during long-term osmotic stimulation raised the question about a possible functional interaction between both substances. (+info)
Diabetes insipidus secondary to penetrating thoracic trauma.
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Three cases of diabetes insipidus following non-cranial trauma are presented. They are believed to be the first of their kind reported. The etiology, pathogenesis and differential diagnosis of diabetes insipidus are discussed. The literature if briefly reviewed and similarities between patients with DI due to long bone trauma with fat embolism, post open heart surgery hypotension, Sheehan's syndrome following postpartum hemorrhage, DI and our own patients are discussed. It is concluded that the diabetes insipidus is caused by selective disruption of posterior pituitary circulation due to fat globules, thrombi and hypovolemia resulting in hypoxia and tissue necrosis. (+info)
Voltage-dependent membrane capacitance in rat pituitary nerve terminals due to gating currents.
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We investigated the voltage dependence of membrane capacitance of pituitary nerve terminals in the whole-terminal patch-clamp configuration using a lock-in amplifier. Under conditions where secretion was abolished and voltage-gated channels were blocked or completely inactivated, changes in membrane potential still produced capacitance changes. In terminals with significant sodium currents, the membrane capacitance showed a bell-shaped dependence on membrane potential with a peak at approximately -40 mV as expected for sodium channel gating currents. The voltage-dependent part of the capacitance showed a strong correlation with the amplitude of voltage-gated Na+ currents and was markedly reduced by dibucaine, which blocks sodium channel current and gating charge movement. The frequency dependence of the voltage-dependent capacitance was consistent with sodium channel kinetics. This is the first demonstration of sodium channel gating currents in single pituitary nerve terminals. The gating currents lead to a voltage- and frequency-dependent capacitance, which can be well resolved by measurements with a lock-in amplifier. The properties of the gating currents are in excellent agreement with the properties of ionic Na+ currents of pituitary nerve terminals. (+info)