Article

delta-Opioid receptors protect from anoxic disruption of Na+ homeostasis via Na+ channel regulation.

Shanghai Research Center for Acupuncture and Meridians, Shanghai, China.
Cellular and Molecular Life Sciences CMLS (impact factor: 6.57). 09/2009; 66(21):3505-16. DOI:10.1007/s00018-009-0136-x pp.3505-16
Source: PubMed

ABSTRACT Hypoxic/ischemic disruption of ionic homeostasis is a critical trigger of neuronal injury/death in the brain. There is, however, no promising strategy against such pathophysiologic change to protect the brain from hypoxic/ischemic injury. Here, we present a novel finding that activation of delta-opioid receptors (DOR) reduced anoxic Na+ influx in the mouse cortex, which was completely blocked by DOR antagonism with naltrindole. Furthermore, we co-expressed DOR and Na+ channels in Xenopus oocytes and showed that DOR expression and activation indeed play an inhibitory role in Na+ channel regulation by decreasing the amplitude of sodium currents and increasing activation threshold of Na+ channels. Our results suggest that DOR protects from anoxic disruption of Na+ homeostasis via Na+ channel regulation. These data may potentially have significant impacts on understanding the intrinsic mechanism of neuronal responses to stress and provide clues for better solutions of hypoxic/ischemic encephalopathy, and for the exploration of acupuncture mechanism since acupuncture activates opioid system.

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Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.

Keywords

activation threshold
 
acupuncture activates opioid system
 
acupuncture mechanism
 
anoxic disruption
 
anoxic Na+ influx
 
DOR antagonism
 
Hypoxic/ischemic disruption
 
hypoxic/ischemic encephalopathy
 
hypoxic/ischemic injury
 
inhibitory role
 
intrinsic mechanism
 
ionic homeostasis
 
Na+ channel regulation
 
Na+ channels
 
neuronal injury/death
 
neuronal responses
 
pathophysiologic change
 
promising strategy
 
sodium currents
 
Xenopus oocytes