Neuronal plasticity as an evolutionary strategy: Implications for neuroprotection in response to hypoxic challenge.

Abstract

Phenotypic plasticity has an important place in evolution because in order to survive in a dynamically changing environment, an organism needs to have a well-adapted set of defense responses, which include pre-emptive and retaliatory phenotypic shifts. From previous research it seems that while only a few vertebrates can survive prolonged periods of hypoxia or anoxia, the greatest physiological challenge occurs when severely diminished oxygen levels are encountered at tropical temperatures. Until recently, all of the neuroprotective strategies examined have been in hypoxia and anoxia tolerant species that evolved their tolerance at temperatures close to freezing. The discovery of a hypoxia and anoxia tolerant reef shark, the epaulette shark (Hemiscyllium ocellatum), has provided a model in which to examine neuroprotective mechanisms that evolved at tropical temperatures. The most susceptible tissues are the heart and brain because their continued metabolic activity rapidly depletes the energy budget. Successfully hypoxia and anoxia tolerant species of fish and turtles have evolved a set of strategies to forestall cell death. These physiological strategies centre on reversibly reprogramming metabolism by reducing energy consumption and increasing glycolysis. This review will focus on the activation of retaliatory and pre-emptive neuroprotective mechanisms that are elicited in the hypoxia and anoxia tolerant tropical epaulette shark to shut down cerebella activity and conserve brain energy charge during an anoxic challenge and will examine changes in the level of the inhibitory neurotransmitter gamma-aminobutyric acid, gamma-aminobutyric acid receptors, the role adenosine and molecular chaperones in forestalling neuronal death.