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Journal Article

Hypothalamic Pituitary Adrenal Axis and Hypothalamic−Neurohypophyseal Responsiveness in Water−Deprived Rats

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons93189

Grinevich,  Valery
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;
Valery Grinevich Group, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Grinevich, V., Ma, X., Verbalis, J., & Aguilera, G. (2001). Hypothalamic Pituitary Adrenal Axis and Hypothalamic−Neurohypophyseal Responsiveness in Water−Deprived Rats. Experimental Neurology, 171(2), 329-341. doi:10.1006/exnr.2001.7784.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0019-A0AF-8
Abstract
The differential effects of osmotic stimulation on magnocellular and parvocellular hypothalamic neurons were studied by analysis of corticotropin−releasing hormone (CRH) and vasopressin (VP) expression in controls and 48−h water−deprived rats subjected to either restraint for 1 h or a single lipopolysaccharide injection (250 μg/100 g). Water deprivation reduced basal CRH mRNA levels but the increments following 4 h of restraint or 6 h lipopolysaccharide (LPS) injection were similar to those in controls. In contrast, water deprivation had no effect on basal VP heteronuclear RNA (hnRNA) and mRNA levels in parvocellular neurons, but responses to restraint or LPS injection were reduced. VP expression in magnocellular paraventricular and supraoptic nuclei, and plasma sodium and vasopressin were higher in water−deprived rats, changes which were unaffected by restraint. LPS injection reduced VP mRNA but not hnRNA levels in magnocellular neurons and increased plasma vasopressin levels only in water−deprived rats independently of changes in plasma sodium. This was accompanied by an increase in vasopressin mRNA content in the posterior pituitary. The data show that the blunted ACTH responses to acute stress during chronic osmotic stimulation are correlated with the inability of parvocellular neurons to increase VP rather than CRH expression. In addition, LPS−induced endotoxemia causes disturbances of the magnocellular vasopressinergic system with an unexpected potentiation of osmotic simulated VP secretion. The lack of increase in VP transcription after LPS and changes in VP mRNA distribution suggest that endotoxemia affect the secretory process at the levels of the neurohypophyseal axon terminal