Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Our earlier autoradiographic work had documented a wide distribution of vasopressin receptors in the hippocampus [R.E. Brinton, K.W. Gee, J.K. Wamsley, T.P. Davis, H.I. Yamamura, Regional distribution of putative vasopressin receptors in rat brain and pituitary by quantitative autoradiography, in: Proc. Natl. Acad. Sci. USA, 81 (1984) pp. 7248-7252; C. Chen, R.D. Brinton, T.J. Shors, R.F. Thompson, [Arg 8]-Vasopressin-induction of long lasting potentiation of synaptic transmission in the dentate gyrus, Hippocampus 3 (1993) 193-203.] which suggested the possibility that receptors for vasopressin were present in both neurons and glia. In the periphery, vasopressin is a potent mitogen in select proliferative cell types [E. Rozengurt, A. Legg, P. Pettican, Vasopressin stimulation of mouse 3T3 cell growth, Proc. Natl. Acad. Sci. USA, 76 (1979) pp. 1284-1287.] which also suggested a possible association between vasopressin receptor activation and the proliferative capacity of astrocytes. We therefore investigated whether vasopressin would induce the expression of the immediate early response gene, NGFI-A (also known as zif/268, ZENK, egr-1, krox 24), which is associated with initiation of mitogenesis [M. Sheng, M.E. Greenberg, The regulation and function of c-fos and other immediate early genes in the nervous system, Neuron, 4 (1990) pp. 477-485.]. Cultured hippocampal glial cells were exposed to vasopressin or a selective V1 vasopressin receptor agonist and in situ hybridization for NGFI-A mRNA was conducted. Results of these experiments demonstrated that vasopressin induced a highly significant dose-dependent increase in the number of cells expressing NGFI-A. Studies to determine the receptor subtype mediating vasopressin induction of NGFI-A were conducted utilizing the specific V1 agonist, [Phe2, Ile3, Orn8]-vasopressin. The V1 receptor agonist induced a highly significant dose dependent increase in the number of grains per NGFI-A positive cell. Time course analysis demonstrated that V1 agonist induction of NGFI-A occurred within 5 min, was maximally induced at 15 min of exposure and exhibited a gradual decline within 30 min of exposure which continued to decline over the 60 min time course. Glial cell responsivity was selective in that vasopressin and V1 agonist induction of NGFI-A occurred in a subpopulation of glial cells. Within a sea of glial cells, vasopressin and V1 agonist would induce islands of NGFI-A positive cells. Results of combined immunocytochemical labeling for the astrocyte specific marker, GFAP, and in situ hybridization for NGFI-A demonstrated that V1 agonist-induced NGFI-A expression occurred in GFAP positive cells. We observed no evidence for V1 agonist induction of NGFI-A in neurons. Collectively, these data document that vasopressin, acting via V1 vasopressin receptors, induces a highly significant increase in NGFI-A expression in select GFAP positive hippocampal astrocytes. To our knowledge, these data are the first report of a vasopressin mediated response in hippocampal glial cells. The potential functional significance of these findings is discussed.
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PMID:Vasopressin-induction of the immediate early gene, NGFI-A, in cultured hippocampal glial cells. 963 May 27

Sleep disruption and other circadian rhythm disturbances are frequently seen in dementia patients. In this study, we examined the suprachiasmatic nucleus (SCN), the putative site of the hypothalamic circadian pacemaker, to determine the nature and degree of pathologic changes caused by severe dementia. Neuropathologic examination indicated that among 30 patients with a clinical history of severe dementia, 22 had Braak and Braak stage V-VI Alzheimer disease, 3 had combined Alzheimer and Parkinson disease, 3 had Pick disease and 2 had severe hippocampal sclerosis. Comparisons were made with a control group composed of 13 age-matched patients with no clinical or pathological evidence of dementia or other CNS disorders. To determine the pathologic involvement within the SCN, human hypothalami were stained with: Nissl, Bielchowsky silver, thioflavin S and specific antibodies directed against vasopressin (VP), neurotensin (NT), neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), beta-amyloid (B/A4) and glial fibrillary acidic protein (GFAP). Pathologic damage was primarily limited to neuronal loss and neurofibrillary tangle formation. Only rare diffuse plaques were noted. The pathologic changes within the SCN were less severe than in the other brain regions. Morphometric analysis was accomplished using a stereological approach to sample the average total number of positively stained neurons and astrocytes in 10 different 0.1mm2 microscopic fields in the dorsal subdivision of the SCN. Patients with Alzheimer disease exhibited a significant decrease in vasopressin (9.75 vs 16.7, p < 0.001) and neurotensin (6.82 vs 9.63, p < 0.002) neurons, as well as a corresponding increase in the GFAP-stained astrocyte/Nissl-stained neuron ratio (0.54 vs 0.10, p < 0.009). These studies provide evidence that both vasopressin and neurotensin neurons are lost in Alzheimer disease, and that the astrocyte/neuron ratio is a reliable indicator of disease-related pathology within the SCN. Taken collectively, our data support the hypothesis that damage to the SCN may be an underlying anatomical substrate for the clinically observed changes in circadian rhythmicity that have been observed in Alzheimer patients.
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PMID:Pathologic evaluation of the human suprachiasmatic nucleus in severe dementia. 1006 11

Microtubule-associated protein-2 is the most abundant microtubule-associated protein in the brain and is responsible for morphogenesis and maintenance of the nervous system. In the present experiments, we have examined the localization of microtubule-associated protein-2 in the hypothalamo-neurohypophysial system of the rat using western blots and immunohistochemistry. Two monoclonal antibodies against microtubule-associated protein-2, antibody C and AP20, were used: antibody C recognizes both the high- and low-molecular-weight isoforms of microtubule-associated protein-2; antibody AP20 specifically detects high-molecular-weight microtubule-associated protein-2 only. Western blot analysis revealed expression of high-molecular-weight microtubule-associated protein-2 in the whole brain, hippocampus and whole hypothalamus. While the supraoptic nucleus expressed only high-molecular-weight microtubule-associated protein-2, the adult posterior pituitary predominantly expressed low-molecular-weight microtubule-associated protein-2, which was also seen in the embryonic whole brain. Light microscopic immunohistochemistry revealed that both antibody C and AP20 intensely stained dendrites of the dendritic and somatic zones in the supraoptic nucleus. Double labeling with antibodies against microtubule-associated protein-2 and oxytocin (or vasopressin) demonstrated that microtubule-associated protein-2 was localized in dendrites of magnocellular neurons in the supraoptic nucleus. In the posterior pituitary, however, antibody C stained fine processes and cell bodies of astrocytes, which were identified by an antibody against glial fibrillary acidic protein. Antibody AP20 also stained fine processes of some astrocytes in the posterior pituitary, but the intensity of immunoreactivity with antibody AP20 was weaker than that with antibody C. This result suggests that microtubule-associated protein-2 in astrocytes of the posterior pituitary is predominantly of the low-molecular-weight type. Moreover, western blots revealed low-molecular-weight microtubule-associated protein-2 of the posterior pituitary at a molecular weight slightly higher than embryonically expressed low-molecular-weight microtubule-associated protein-2, indicating that low-molecular-weight microtubule-associated protein-2 in the posterior pituitary is possibly the isoform microtubule-associated protein-2d. The present results demonstrate that astrocytes in the posterior pituitary of adult rats still retain the ability to express the immature variant of microtubule-associated protein-2, low-molecular-weight microtubule-associated protein-2, and its expression is probably linked to structural plasticity.
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PMID:Microtubule-associated protein-2 in the hypothalamo-neurohypophysial system: low-molecular-weight microtubule-associated protein-2 in pituitary astrocytes. 1033 37

A striking example of the capacity of adult astrocytes to undergo reversible morphological changes in response to stimuli which enhance neuronal activity is offered by astrocytes of the adult hypothalamo-neurohypophysial system (HNS). The HNS is composed of magnocellular neurons secreting the neurohormones oxytocin and vasopressin from axon terminals in the neurohypophysis. Upon activation of HNS secretion, glial coverage of oxytocin neurons significantly diminishes and their surfaces become extensively juxtaposed. These glial changes are invariably accompanied by structural synaptic remodelling resulting in increased numbers of GABAergic, glutamatergic, and noradrenergic afferents. In the neurohypophysis, they result in an enhanced neurohemal contact area. HNS glia in the adult continue to display "embryonic" features that may allow such activity-dependent structural plasticity. For example, supraoptic astrocytes display a radial glia-like morphology and continue to express vimentin, together with GFAP. All HNS astrocytes secrete extracellular matrix glycoproteins, like tenascin-C; they also express high levels of polysialylated NCAM or PSA-NCAM and the glycoprotein F3, molecules considered essential for neuronal-glial interactions in the developing and lesioned CNS. HNS expression of most of these proteins does not visibly vary under different conditions of neurohormone secretion. We consider them as permissive factors, therefore, allowing HNS cells to undergo remodeling whenever the proper stimuli intervene. In the hypothalamic nuclei, one such stimulus is oxytocin itself which, in synergy with steroids, can induce neuronal-glial remodelling; adrenaline does so in the neurohypophysis.
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PMID:Contribution of astrocytes to activity-dependent structural plasticity in the adult brain. 1063 28

Ultrastructural and immunohistochemical studies of the supraoptic nucleus (SON) have provided evidence that retraction and extension of astrocytic processes from between magnocellular neuroendocrine cells (MNCs) likely plays a role in the release of oxytocin, and/or vasopressin, that accompanies parturition, lactation and dehydration. The present study estimates the surface density (Sv) of glial fibrillary acidic protein (GFAP)-immunoreactivity, predominantly in astrocytic processes, in the SON of normally hydrated, dehydrated and rehydrated rats. The Sv of GFAP processes in dehydrated rats was significantly reduced compared with control levels. Rehydration returned Sv to control levels. The reversible reduction in Sv indicates that the previously observed reduction in optical density is due to a rearrangement of astrocyte processes in the SON which occurs at the same time as the selective functional activation of MNCs.
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PMID:The surface density of glial fibrillary acidic protein immunopositive astrocytic processes in the rat supraoptic nucleus is reversibly altered by dehydration and rehydration. 1064 97

The intrinsic properties of the suprachiasmatic nucleus (SCN), the site of the main circadian pacemaker in mammals, have recently been studied in vitro by means of organotypic slice culturing. So far, only neonatal rats and mice have been used for such developmental and functional analyses of the isolated pacemaker. Here, the authors present a comparative developmental study of the SCN of voles, rats, and hamsters in organotypic slice cultures. In contrast to strictly circadian organization of behavior in rats and hamsters, common voles (Microtus arvalis) are characterized by large variability in the strength of circadian organization of behavior. It is not known to what extent this variability is reflected in the intrinsic features of the SCN. Cultures were prepared from rat, hamster, and vole pups (6 to 9 days old) for the purpose of species comparison. In addition, the authors studied the relation between age and development in cultures from pup (7 to 10 days old), juvenile (15 to 16 days old), and young adult (1 to 2 months old) voles. In contrast to the situation in rat and hamster, the most striking feature in neonatal voles is the variability in shape of the final, fully developed culture and its poor resemblance with the in vivo SCN. The SCN of adult voles, however, could be cultured successfully while retaining its morphological organization seen in situ. Phase-contrast microscopy and immunocytochemical staining for vasopressin and glial fibrillary acidic protein revealed that cultures of pup and juvenile voles still have potential for neurogenesis and morphological reorganization. Young voles, therefore, can serve as a model to study the developmental establishment of a functional circadian pacemaker, while adult voles allow the study of intrinsic pacemaker properties in relation to previously recorded behavior of the donor and aging-related pacemaker dysfunction.
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PMID:The suprachiasmatic nucleus in organotypic slice cultures of the common vole (Microtus arvalis): comparison of development with rat and hamster and the effect of age. 1067 15

Pituicytoma is a rare, poorly characterized tumor of the sella and suprasellar region that is distinct morphologically from other local tumors and is thought to be derived from neurohypophyseal pituicytes. Clinical data, neuroimaging studies, and microsections were reviewed from nine such low-grade gliomas. Immunostains for glial, neuronal, and proliferation markers were performed on all nine tumors and six control neurohypophyses. Three tumors were studied ultrastructurally. Six men and three women, age 30 to 83 years (mean, 48 years), presented with visual symptoms, headache, or hypopituitarism. Magnetic resonance images showed solid, discrete, contrast-enhancing masses, four within the sella and five in the suprasellar space. The tumors consisted of sheets and/or fascicles of plump spindle cells with slightly fibrillar cytoplasm and slightly pleomorphic, oval-to-elongate nuclei with pinpoint nucleoli. Extracellular mucin was prominent in one tumor. Rosenthal fibers, granular bodies, and Herring bodies (granular axonal dilatations characteristic of the normal neurohypophysis) were lacking. Mitoses were rare or absent. MIB-1 labeling indices were low (0.5-2%). Tumor cells were strongly reactive for vimentin and S-100 protein, variably positive for glial fibrillary acidic protein, and nonreactive for synaptophysin and neurofilament protein. Cytoplasm varied in electron density and contained intermediate filaments. Neither meningothelial nor ependymal features were noted. Two tumors recurred at 20 and 26 months after subtotal resection, but none of the six completely resected tumors have done so. Pituicytomas are discrete, largely noninfiltrative low-grade gliomas of the sellar region that occur in adults. Their histologic appearance is distinct from pilocytic and ordinary, infiltrative astrocytomas. The distinction between pituicytoma and normal neurohypophysis is aided by the latter's content of axons, Herring bodies, and perivascular anucleate zones rich in axonal terminations. Although curable by total excision, subtotal resection can be associated with recurrence.
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PMID:Pituicytoma: a distinctive low-grade glioma of the neurohypophysis. 1071 49

Enzymatically dispersed cells, isolated from adult female rat neural lobes, were cultured for 7 days. Routine cultures showed pituicytes with compact, sometimes ovoid, cell bodies. The cytoplasmic processes of these cells exhibited several varicosities and made contact with neighboring cells forming networks. The cultured pituicytes were immunocytochemically characterized using antisera to glial fibrillary acidic protein and to S-100. Most pituicytes, when exposed during culture to oxytocin (OXY) and vasopressin (VP; 1 microM each), were devoid of their characteristic processes. Immunocytochemical staining for OXY or VP revealed that the pituicytes were capable of incorporating these hormones during culture. In cultures without added hormones, no significant staining reaction for OXY or VP could be detected. The lack of projections in pituicytes exposed to the hormones during culture is in agreement with the morphological changes observed by other authors in situ after acute hormone release. The uptake of OXY and VP may be indicative for a regulatory mechanism, by which the pituicytes control the amount of hormones present in the intercellular space.
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PMID:Hormone uptake and morphological changes in cultured pituicytes exposed to oxytocin and vasopressin. 1090 30

Previous studies suggest that activation of N-methyl-D-aspartate (NMDA) receptors facilitates phasic firing and spike clustering displayed by magnocellular neuroendocrine cells (MNCs) of the supraoptic (SON) and paraventricular nucleus of the hypothalamus (PVN). Osmotic stimulation produces similar activity patterns which, in turn, can lead to enhanced release of vasopressin and oxytocin from MNCs. Our laboratory has shown that dehydration regulates the expression of the NMDA receptor subunits, NR1 and NR2B, in the SON and PVN, suggesting their involvement in osmoregulation. In the present study, we examined the cellular localization of NR2B, one of the glutamate-binding subunits of the NMDA receptor, with an NR2B-specific antibody. Using double-label immunohistochemistry and three different detection methods with metallic, peroxidase, and fluorescence markers, it was found that both vasopressin and oxytocin-producing MNC populations synthesize NR2B. The incidence of NR2B colocalization with vasopressin-neurophysin in the SON and lateral magnocellular PVN (PVL) was 0.95 and 0.91, respectively. For oxytocin-neurophysin, the corresponding values were 0.97 and 0.95, respectively. Furthermore, the extent of colocalization in MNCs of the SON, PVL, retrochiasmatic SON, and accessory neurosecretory nuclei was similar. Astrocytes associated with the SON, and identified with antibodies targeting glial fibrillary acidic protein (GFAP) or vimentin, were not colabeled with NR2B. Our results demonstrate that NR2B protein is expressed by almost all MNCs and that it is equally prevalent in vasopressinergic and oxytocinergic populations of various magnocellular neuroendocrine nuclei supporting a role of NMDA receptors in MNC-mediated neurosecretory processes. Although NR2B may form part of functional NMDA receptors on MNCs, it is probably not present on astrocytes associated with nearby MNCs.
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PMID:Immunolabeling reveals cellular localization of the N-methyl-D-aspartate receptor subunit NR2B in neurosecretory cells but not astrocytes of the rat magnocellular nuclei. 1104 93

The suprachiasmatic nucleus (SCN) is the central circadian pacemaker governing the circadian rhythm of locomotor activity in mammals. The mammalian retina also contains circadian oscillators, but their roles are unknown. To test whether the retina influences circadian rhythms of locomotor behavior, the authors compared the activity of bilaterally enucleated hamsters with the activity of intact controls held in constant darkness (DD). Enucleated hamsters showed a broader range of free-running periods (tau) than did intact hamsters held for the same length of time in DD. This effect was independent of the age at enucleation (on postnatal days 1, 7, or 28). The average tau of intact animals kept in DD from days 7 or 28 was significantly longer than that of intact animals kept in DD from day 1 or any of the enucleated groups. This indicates that early exposure to light-dark cycles lengthens the tau and that the eye is required to maintain this effect even in DD. These data suggest that hypothalamic circadian pacemakers may interact continuously with the retina to determine the tau of locomotor activity. Enucleation caused a large decrease in glial fibrillary acidic protein in the SCN but has no (or slight) effects on calbindin, neuropeptide Y, vasopressin, or vasoactive intestinal polypeptide, which suggests that enucleation does not produce major damage to the SCN, an interpretation that is supported by the fact that enucleated animals retain robust circadian rhythmicity. The presence of an intact retina appears to contribute to system-level circadian organization in mammals perhaps as a consequence of interaction between its circadian oscillators and those in the SCN.
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PMID:Interaction of the retina with suprachiasmatic pacemakers in the control of circadian behavior. 1216 48


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