Abstract
Oxytocin protects against ischemia-induced inflammation and oxidative stress, and is associated with GABA (γ-aminobutyric acid, an inhibitory neurotransmitter) signaling transduction in neurons. However, the molecular mechanism by which oxytocin affords neuroprotection, especially the interaction between oxytocin receptor and GABAA receptor (GABAAR), remains to be elucidated. Primary rat neural cells were exposed to oxytocin before induction of experimental acute stroke model via oxygen-glucose deprivation-reperfusion (OGD/R) injury. Pretreatment with oxytocin increased cell viability, decreased the cell damage against oxidative stress, and prevented the release of high mobility group box1 during OGD/R. However, introduction of oxytocin during OGD/R did not induce neuroprotection. Although oxytocin did not affect the glutathione-related cellular metabolism before OGD, oxytocin modulated the expression levels of GABAAR subunits, which function to remove excessive neuronal excitability via chloride ion influx. Oxytocin-pretreated cells significantly increased the chloride ion influx in response to GABA and THIP (δ-GABAAR specific agonist). This study provides evidence that oxytocin regulated GABAAR subunits in affording neuroprotection against OGD/R injury.
Highlights
Oxytocin protects against ischemia-induced inflammation and oxidative stress, and is associated with GABA (γ-aminobutyric acid, an inhibitory neurotransmitter) signaling transduction in neurons
We found that oxytocin-induced GABAA receptor (GABAAR) subunit modification is a predominant factor in conferring neuroprotection against oxygen-glucose deprivation (OGD)
Our present results demonstrated that oxytocin reduced ischemic stroke deficits likely by modulating specific GABAAR subtype signal transduction[14], which parallels studies showing that oxytocin improves stroke outcomes via social interaction pathways[18]
Summary
Oxytocin protects against ischemia-induced inflammation and oxidative stress, and is associated with GABA (γ-aminobutyric acid, an inhibitory neurotransmitter) signaling transduction in neurons. Primary rat neural cells were exposed to oxytocin before induction of experimental acute stroke model via oxygen-glucose deprivation-reperfusion (OGD/R) injury. Oxytocin did not affect the glutathione-related cellular metabolism before OGD, oxytocin modulated the expression levels of GABAAR subunits, which function to remove excessive neuronal excitability via chloride ion influx. Oxytocin-pretreated cells significantly increased the chloride ion influx in response to GABA and THIP (δ-GABAAR specific agonist). This study provides evidence that oxytocin regulated GABAAR subunits in affording neuroprotection against OGD/R injury. Interleukin (IL)-1β, IL-6, interferon τ, and oxytocin regulate the expression levels of oxytocin receptors[4]. The equilibrium shift of GABAAR subtype expression pattern is a key control point for the determination of receptor diversity of the neuronal plasma membrane. GABAARs on neuronal cell membrane are decreased when exposed to oxygen-glucose deprivation (OGD), www.nature.com/scientificreports/
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