ArticlePloS one2014
Reduction in neural performance following recovery from anoxic stress is mimicked by AMPK pathway activation.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 18 citations in OpenAlex.
- From insult to hyperexcitability: pharmacological targeting of MyD88 and JAK/STAT3 pathways in epilepsy.Inflammopharmacology · 2026Review
- Low Glycolysis Is Neuroprotective during Anoxic Spreading Depolarization (SD) and Reoxygenation in Locusts.eNeuro · 2023Article
- Neural shutdown under stress: an evolutionary perspective on spreading depolarization.Journal of neurophysiology · 2020Review
- Chill coma in the locust, Locusta migratoria, is initiated by spreading depolarization in the central nervous system.Scientific reports · 2017Article
- Octopamine stabilizes conduction reliability of an unmyelinated axon during hypoxic stress.Journal of neurophysiology · 2016Article
- Ionic mechanisms maintaining action potential conduction velocity at high firing frequencies in an unmyelinated axon.Physiological reports · 2016Article
- Na+-K+-ATPase trafficking induced by heat shock pretreatment correlates with increased resistance to anoxia in locusts.Journal of neurophysiology · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nervous systems are energetically expensive to operate and maintain. Both synaptic and action potential signalling require a significant investment to maintain ion homeostasis. We have investigated the tuning of neural performance following a brief period of anoxia in a well-characterized visual pathway in the locust, the LGMD/DCMD looming motion-sensitive circuit. We hypothesised that the energetic cost of signalling can be dynamically modified by cellular mechanisms in response to metabolic stress. We examined whether recovery from anoxia resulted in a decrease in excitability of the electrophysiological properties in the DCMD neuron. We further examined the effect of these modifications on behavioural output. We show that recovery from anoxia affects metabolic rate, flight steering behaviour, and action potential properties. The effects of anoxia on action potentials can be mimicked by activation of the AMPK metabolic pathway. We suggest this is evidence of a coordinated cellular mechanism to reduce neural energetic demand following an anoxic stress. Together, this represents a dynamically-regulated means to link the energetic demands of neural signaling with the environmental constraints faced by the whole animal.
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