Meeting Abstract
In most organisms, even brief episodes of low oxygen supply can cause irreparable damages to vital organs, such as the brain and heart. The annual killifish (Austrofundulus limnaeus) survives in ephemeral ponds and their embryos have the remarkable ability to tolerate anoxia for months. In addition, A. limnaeus must also contend with the seasonal dehydration of their ponds, which they survive through mechanisms that likely highly limit gas exchange. We propose that anoxia tolerance is a pre-adaptation that allowed the evolution of dehydration tolerance. Thus, we predict that A. limnaeus embryos exposed to dehydrating conditions will show similar responses at the molecular level to embryos exposed to anoxia. When exposed to anoxia, embryos of A. limnaeus respond by producing significant amounts of γ-aminobutyric acid (GABA) and lactate. When exposed to desiccation, embryos of A. limnaeus also respond by producing significant amounts of GABA, though at a slower rate than when exposed to anoxia. This study aims to understand the role of GABA and lactate in supporting the metabolic response to anoxia and desiccation across development. In addition, this study explores the roles of glutamate decarboxylase (GAD) activity and metabolic rate in determining the rate of GABA and lactate accumulation in response to anoxia and desiccation. GABA has been found to provide excitatory actions in the developing vertebrate nervous system, but conversely, typically functions as an inhibitory neurotransmitter in adults. The high levels of GABA accumulated during anoxia and desiccation in A. limnaeus embryos suggests GABA may serve a purpose other than as a neurotransmitter when embryos are under stress.
