Publication Date
2006
Document Type
Thesis
Committee Members
Jay Dean (Advisor)
Degree Name
Master of Science (MS)
Abstract
The NTS is one of many sites of chemoreception meaning that it responds to changes in CO2 and pH. NTS neurons also acidify approximately 0.13 pH units in response to hypoxia. Experiments involved brainstem slices exposed to a control hypoxic bout followed by hypoxia in conjunction with different drugs. The drugs included fluorocitrate, 4-hydroxycinnamate, oxygen-glucose deprivation and iodoacetate. Iodoacetate produced the strongest blunting of the hypoxia-induced acidification and decreased the response by ~53%. Results from the studies using the superoxide probe DHE showed an increase in the levels of ROS during the hypoxic exposure prior to reoxygenation. Two ROS scavengers melatonin and manganese(III)tetrakis(1-methylpyridyl) porphyrin pentachloride both reduced the increase in ROS by ~30%. In conclusion, the hypoxia-induced acidification seems to be due to lactate production which is proposed to come from neuronal sources as the glial source of lactate was ruled out with the fluorocitrate and 4-hydroxycinnamate studies.
Page Count
116
Department or Program
Department of Neuroscience, Cell Biology & Physiology
Year Degree Awarded
2006
Copyright
Copyright 2006, all rights reserved. This open access ETD is published by Wright State University and OhioLINK.
