ArticleJournal of neurophysiology2014
Na+-K+-ATPase trafficking induced by heat shock pretreatment correlates with increased resistance to anoxia in locusts.
Article in Journal of neurophysiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 39 citations in OpenAlex.
- Na,K-ATPase α1 and β-subunits show distinct localizations in the nervous tissue of the large milkweed bug.Cell and tissue research · 2022Article
- Analysis of temperature-dependent abnormal bursting patterns of neurons inThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2020Article
- Neural shutdown under stress: an evolutionary perspective on spreading depolarization.Journal of neurophysiology · 2020Review
- Spreading depolarization triggered by elevated potassium is weak or absent in the rodent lower brain.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Mechanisms of spreading depolarization in vertebrate and insect central nervous systems.Journal of neurophysiology · 2016Review
- 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
- Heat shock response and homeostatic plasticity.Frontiers in cellular neuroscience · 2015Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The sensitivity of insect nervous systems to anoxia can be modulated genetically and pharmacologically, but the cellular mechanisms responsible are poorly understood. We examined the effect of a heat shock pretreatment (HS) on the sensitivity of the locust (Locusta migratoria) nervous system to anoxia induced by water immersion. Prior HS made locusts more resistant to anoxia by increasing the time taken to enter a coma and by reducing the time taken to recover the ability to stand. Anoxic comas were accompanied by surges of extracellular potassium ions in the neuropile of the metathoracic ganglion, and HS reduced the time taken for clearance of excess extracellular potassium ions. This could not be attributed to a decrease in the activity of protein kinase G, which was increased by HS. In homogenates of the metathoracic ganglion, HS had only a mild effect on the activity of Na(+)-K(+)-ATPase. However, we demonstrated that HS caused a threefold increase in the immunofluorescent localization of the α-subunit of Na(+)-K(+)-ATPase in metathoracic neuronal plasma membranes relative to background labeling of the nucleus. We conclude that HS induced trafficking of Na(+)-K(+)-ATPase into neuronal plasma membranes and suggest that this was at least partially responsible for the increased resistance to anoxia and the increased rate of recovery of neural function after a disturbance of K(+) homeostasis.
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