Electronic Theses and Dissertations

Identifier

1032

Date

2014

Date of Award

4-21-2014

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.

Comments

Data is provided by the student.

Library Comment

dissertation or thesis originally submitted to the local University of Memphis Electronic Theses & dissertation (ETD) Repository.

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