Subject Area

Biochemistry and Molecular Biology

Description

Annual killifish (Austrofundulus limnaeus) live in temporary ponds in Venezuela and experience drastic changes in their environment that cause their ponds to dry up. This species survives by producing drought- and anoxia-tolerant embryos that are deposited in the mud. Embryos survive these conditions by entering metabolic dormancy (diapause) until environmental signals break their dormancy and they continue developing. In order to survive anoxia, embryos rely exclusively on anaerobic metabolism, which leads to abundant lactate accumulation. Previous research has shown that the production and degradation of the neurotransmitter γ-aminobutyric acid (GABA) is crucial for long-term anoxia survival. This study explores the role of lactate and GABA metabolism in anoxia tolerance. To test this, we exposed embryo-derived cells (WS40NE) in anoxia to three treatments: anoxia preconditioning, lactate preconditioning, and GABA supplementation. For all treatments, cell survival was monitored, and extracellular lactate levels were measured. Compared to the control, cells exposed to lactate and GABA proliferated at a higher rate, whereas the anoxia preconditioned treatment proliferated at a lower rate. Rate of lactate accumulation was dependent on time spent in anoxia as well as whether cell media was changed. Media changes led to higher rates of lactate production compared to cells in static media. Understanding survival of cells during anoxia may give insight to how human conditions, such as strokes, can be avoided or damage can be reversed.

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May 17th, 12:00 AM

GABA and lactate preconditioning increases cell division in annual killifish cell line during anoxia

Annual killifish (Austrofundulus limnaeus) live in temporary ponds in Venezuela and experience drastic changes in their environment that cause their ponds to dry up. This species survives by producing drought- and anoxia-tolerant embryos that are deposited in the mud. Embryos survive these conditions by entering metabolic dormancy (diapause) until environmental signals break their dormancy and they continue developing. In order to survive anoxia, embryos rely exclusively on anaerobic metabolism, which leads to abundant lactate accumulation. Previous research has shown that the production and degradation of the neurotransmitter γ-aminobutyric acid (GABA) is crucial for long-term anoxia survival. This study explores the role of lactate and GABA metabolism in anoxia tolerance. To test this, we exposed embryo-derived cells (WS40NE) in anoxia to three treatments: anoxia preconditioning, lactate preconditioning, and GABA supplementation. For all treatments, cell survival was monitored, and extracellular lactate levels were measured. Compared to the control, cells exposed to lactate and GABA proliferated at a higher rate, whereas the anoxia preconditioned treatment proliferated at a lower rate. Rate of lactate accumulation was dependent on time spent in anoxia as well as whether cell media was changed. Media changes led to higher rates of lactate production compared to cells in static media. Understanding survival of cells during anoxia may give insight to how human conditions, such as strokes, can be avoided or damage can be reversed.