Increase of Lactate Concentration During Spreading Depression

Lima, S. M.; Rodrigues, B. C.; Lara, J. N.; Nogueira, G.S.; Almeida, Antonio Carlos; Rodrigues, Antônio Márcio

doi:10.1007/978-3-030-70601-2_328

Cited by 1 publication

(1 citation statement)

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“…In locusts, glycogen is depleted in the CNS following anoxia, suggesting heightened glucose utilization during anoxic SD (Hochachka, 1993). Anaerobic glycolysis is often erroneously described as the source of lowered cellular pH during SD via "lactic acid" production (Bo et al, 2020;Grech et al, 2021;Lima et al, 2022;Rossi et al, 2007;Tóth et al, 2020;Uzdensky, 2019); however, only lactate is formed which does not contribute to acidification (Robergs et al, 2018). Nonetheless, few studies have examined the impact of glycolysis and glycolytically-derived energy on SD in metabolically-challenged tissues, and the conclusions have been difficult to reconcile.…”

Section: Introductionmentioning

confidence: 99%

Low Glycolysis Is Neuroprotective during Anoxic Spreading Depolarization (SD) and Reoxygenation in Locusts

Wang (王宇扬),

Little,

Aristizabal

et al. 2023

eNeuro

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Migratory locusts enter a reversible hypometabolic coma to survive environmental anoxia, wherein the cessation of CNS activity is driven by spreading depolarization (SD). While glycolysis is recognized as a crucial anaerobic energy source contributing to animal anoxia tolerance, its influence on the anoxic SD trajectory and recovery outcomes remains poorly understood. We investigated the effects of varying glycolytic capacity on adult female locust anoxic SD parameters, using glucose or the glycolytic inhibitors 2-deoxy-d-glucose (2DG) or monosodium iodoacetate (MIA). Surprisingly, 2DG treatment shared similarities with glucose yet had opposite effects compared with MIA. Specifically, although SD onset was not affected, both glucose and 2DG expedited the recovery of CNS electrical activity during reoxygenation, whereas MIA delayed it. Additionally, glucose and MIA, but not 2DG, increased tissue damage and neural cell death following anoxia-reoxygenation. Notably, glucose-induced injuries were associated with heightened CO2output during the early phase of reoxygenation. Conversely, 2DG resulted in a bimodal response, initially dampening CO2output and gradually increasing it throughout the recovery period. Given the discrepancies between effects of 2DG and MIA, the current results require cautious interpretations. Nonetheless, our findings present evidence that glycolysis is not a critical metabolic component in either anoxic SD onset or recovery and that heightened glycolysis during reoxygenation may exacerbate CNS injuries. Furthermore, we suggest that locust anoxic recovery is not solely dependent on energy availability, and the regulation of metabolic flux during early reoxygenation may constitute a strategy to mitigate damage.

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