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)

Astroglial-neuronal interactions are important in brain functions. However, roles of glial fibrillary acidic protein (GFAP) in this interaction remain unclear in acute physiological processes. We explored this issue using the supraoptic nucleus (SON) in lactating rats. At first, we identified the essential role of astrocytes in the milk-ejection reflex (MER) by disabling astrocytic functions via intracerebroventricular application of l-aminoadipic acid (l-AAA). l-AAA blocked the MER and reduced GFAP levels in the SON. In brain slices, l-AAA suppressed oxytocin (OT) neuronal activity and EPSCs. Suckling reduced GFAP in immunocytochemical images and in Western blots, reductions that were partially reversed after the MER. OT, the dominant hormone mediating the MER, reduced GFAP expression in brain slices. Tetanus toxin suppressed EPSCs but did not influence OT-reduced GFAP. Protease inhibitors did not influence OT-reduced GFAP images but blocked the degradation of GFAP molecules. In the presence of OT, transient 12 mm K(+) exposure, simulating effects of synchronized bursts before the MER, reversed OT-reduced GFAP expression. Consistently, suckling first reduced and then increased the expression of aquaporin 4, astrocytic water channels coupled to K(+) channels. Moreover, GFAP molecules were associated with astrocytic proteins, including aquaporin 4, actin, and glutamine synthetase and serine racemase. GFAP-aquaporin 4 association decreased during initial suckling and increased after the MER, whereas opposite changes occurred between GFAP and actin. MER also decreased the association between GFAP and glutamine synthetase. These results indicate that suckling elicits dynamic glial neuronal interactions in the SON; GFAP plasticity dynamically reflects OT neuronal activity.
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PMID:Astrocytic plasticity and patterned oxytocin neuronal activity: dynamic interactions. 1921 81

The vasopressin- and oxytocin-degrading enzyme insulin-regulated aminopeptidase (IRAP) is expressed in various organs including the brain. However, knowledge about its presence in human hypothalamus is fragmentary. Functionally, for a number of reasons (genetic linkage, hydrolysis of oxytocin and vasopressin, its role as angiotensin IV receptor in learning and memory and others) IRAP might play a role in schizophrenia. We studied the regional and cellular localization of IRAP in normal human brain with special emphasis on the hypothalamus and determined numerical densities of IRAP-expressing cells in the paraventricular, supraoptic and suprachiasmatic nuclei in schizophrenia patients and controls. By using immunohistochemistry and Western blot analysis, IRAP was immunolocalized in postmortem human brains. Cell countings were performed to estimate numbers and numerical densities of IRAP immunoreactive hypothalamic neurons in schizophrenia patients and control cases. Shape, size and regional distribution of IRAP-expressing cells, as well the lack of co-localization with the glia marker glutamine synthetase, show that IRAP is expressed in neurons. IRAP immunoreactive cells were observed in the hippocampal formation, cerebral cortex, thalamus, amygdala and, abundantly, hypothalamus. Double labeling experiments (IRAP and oxytocin/neurophysin 1, IRAP with vasopressin/neurophysin 2) revealed that IRAP is present in oxytocinergic and in vasopressinergic neurons. In schizophrenia patients, the numerical density of IRAP-expressing neurons in the paraventricular and the suprachiasmatic nuclei is significantly reduced, which might be associated with the reduction in neurophysin-containing neurons in these nuclei in schizophrenia. The pathophysiological role of lowered hypothalamic IRAP expression in schizophrenia remains to be established.
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PMID:Insulin-regulated aminopeptidase immunoreactivity is abundantly present in human hypothalamus and posterior pituitary gland, with reduced expression in paraventricular and suprachiasmatic neurons in chronic schizophrenia. 2803 72