Lithium Protects against Anesthesia-induced Developmental Neuroapoptosis
Open Access
- 1 April 2009
- journal article
- meeting abstracts
- Published by Ovid Technologies (Wolters Kluwer Health) in Anesthesiology
- Vol. 110 (4), 862-868
- https://doi.org/10.1097/aln.0b013e31819b5eab
Abstract
Ethanol and anesthetic drugs trigger neuroapoptosis in the developing mouse brain. Recently, it was found that ethanol-induced neuroapoptosis is preceded by suppressed phosphorylation of extracellular signal-regulated protein kinase (ERK), and lithium counteracts both the phosphorylated ERK suppressant action and ethanol-induced neuroapoptosis. The present study was undertaken to address the following questions: 1) Do ketamine and propofol mimic ethanol in suppressing ERK phosphorylation? 2) If they do, does lithium prevent this suppressant action, and also prevent these anesthetic drugs from triggering neuroapoptosis? Postnatal day 5 mice were treated with propofol, ketamine, lithium, a combination of propofol or ketamine and lithium or saline and their brains prepared for western blot analysis or histology. For western blot, cytosolic lysates of caudate putamen were analyzed for expression of phosphorylated ERK and phosphorylated serine/threonine-specific protein kinase. For histology, brains were stained immunohistochemically with antibodies to activated caspase-3 and the density of activated caspase-3 positive cells determined. Ketamine and propofol suppressed phosphorylated ERK, and lithium counteracted both the phosphorylated ERK suppressant action and neuroapoptotic action of these anesthetic drugs. If further testing finds lithium to be safe for use in pediatric/obstetric medicine, administration of a single dose of lithium prior to anesthesia induction may be a suitable means of mitigating the risk of anesthesia-induced developmental neuroapoptosis.Keywords
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