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 impose highly limited 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 large amounts (> 10mM) of the neurotransmitter γ -aminobutyric acid (GABA). 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. GABA has been found to provide excitatory actions in the developing vertebrate nervous system, but conversely, typically functions as an inhibitory neurotransmitter in adults. We hypothesize that A. limnaeus embryos produce GABA as a metabolic end-product during exposures to anoxia, as well as during exposures to desiccation. 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.
