Electronic Theses and Dissertations
Identifier
1032
Date
2014
Document Type
Thesis
Degree Name
Master of Science
Major
Psychology
Committee Chair
Guy Mittleman
Committee Member
Charles D Blaha
Committee Member
J Gayle Beck
Committee Member
William Farmer
Abstract
Impaired responsivity to hypercapnia or hypoxia is commonly considered a mechanism of failure in Sudden Infant Death Syndrome (SIDS). We used a model of developmental cerebellar Purkinje cell loss to determine if such loss influenced compensatory ventilatory responses to hypercapnic and hypoxic challenges. Twenty-four Lurcher mutant mice and wildtype controls were sequentially exposed to 2% increases in CO2 (0%-8%) or 2% reductions in O2 (21%-13%) for four-minutes, with return to room air between each exposure. Whole-body plethysmography was used to continuously monitor tidal volume and breath frequency. Tidal volume increases to CO2 elevation were reduced in Mutants, and slower to recover. Increased breathing rates to hypercapnia were also lower in Mutants, and were unable to be maintained in recovery, except for very high (8%) CO2 levels. Less pronounced ventilatory responses emerged to hypoxia. Since cerebellar neuropathology appears in SIDS victims, developmental cerebellar neuropathology may contribute to SIDS vulnerability.
Library Comment
Dissertation or thesis originally submitted to the local University of Memphis Electronic Theses & dissertation (ETD) Repository.
Recommended Citation
Calton, Michele Ann, "Cerebellar Purkinje Cell Loss in Developing Lurcher Mice Influences Respiratory Compensatory Responses to Acute Hypercapnia and Hypoxia" (2014). Electronic Theses and Dissertations. 873.
https://digitalcommons.memphis.edu/etd/873
Comments
Data is provided by the student.