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• W2476844384 abstract "Mammalian cells are vulnerable to the external salt-water balance, and the effects of osmotic pressure. If an unprotected cell is placed in water with too little salt it will swell and burst, but if there is too much salt then the cell will shrivel and die; water is drawn from a compartment where the salt concentration is low to a compartment where it is high, equalizing the concentrations. Mammals must therefore maintain the concentration of electrolytes (especially Na+) in the extracellular fluid within narrow limits, and to do so they depend on specialized neurons that can detect changes in the osmotic pressure of the extracellular fluid. These “osmoreceptive” neurons have stretch-sensitive channels in their membranes that allow them to respond to osmotically induced changes in volume with changes in electrical activity. These osmoreceptors regulate the endocrine and behavioral responses that are appropriate for body fluid homeostasis - thirst, sodium excretion, antidiuresis, and plasma volume. The magnocellular vasopressin neurons are both osmoreceptors themselves, and also receive input from other osmoreceptors. They respond to increases in extracellular osmotic pressure by secreting vasopressin into the bloodstream, which acts as an antidiuretic hormone at the kidneys to concentrate the urine and hence reduce water loss. At the same time, the vasopressor actions that give vasopressin its name compensate for a reduction in body water by constricting blood vessels. In all mammals, vasopressin secretion is linearly proportional to plasma osmotic pressure over a wide dynamic range above a “set point,” and, under conditions of water deprivation, vasopressin secretion might need to be elevated for several days. Over the last 40 years, vasopressin cells have been the object of intense experimental study, and we probably know as much or more about them as about any neurons in the brain. One particularly intriguing feature is that these neurons show a distinctive “phasic” pattern of firing activity. Computational modeling can help us to understand how and importantly, why this pattern is generated." @default.
• W2476844384 created "2016-08-23" @default.
• W2476844384 creator A5047874096 @default.
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• W2476844384 date "2016-04-11" @default.
• W2476844384 modified "2023-10-18" @default.
• W2476844384 title "Modeling Spiking and Secretion in the Magnocellular Vasopressin Neuron" @default.
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• W2476844384 doi "https://doi.org/10.1002/9781119159438.ch5" @default.
• W2476844384 hasPublicationYear "2016" @default.
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