Date of Award
Master of Science
Charles D Blaha
J Gayle Beck
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.
dissertation or thesis originally submitted to the local University of Memphis Electronic Theses & dissertation (ETD) Repository.
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.