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Am J Physiol Cell Physiol 282: C1225-C1234, 2002; doi:10.1152/ajpcell.00226.2001
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Vol. 282, Issue 6, C1225-C1234, June 2002

Neuroprotective role of delta -opioid receptors in cortical neurons

Junhui Zhang*, Geoffrey Thomas Gibney*, Peng Zhao, and Ying Xia

Department of Pediatrics, Yale University, New Haven, Connecticut 06520

We recently demonstrated that delta -opioid receptor (DOR) activation protects cortical neurons against glutamate-induced injury. Because glutamate is a mediator of hypoxic injury in neurons, we hypothesized that DOR is involved in neuroprotection during O2 deprivation and that its activation/inhibition may alter neuronal susceptibility to hypoxic stress. In this work, we tested the effect of opioid receptor activation and inhibition on cultured cortical neurons in hypoxia (1% O2). Cell injury was assessed by lactate dehydrogenase release, morphology-based quantification, and live/dead staining. Our results show that 1) immature neurons (days 4 and 6) were not significantly injured by hypoxia until 72 h of exposure, whereas day 8 neurons were injured after only 24-h hypoxia; 2) DOR inhibition (naltrindole) caused neuronal injury in both day 4 and day 8 normoxic cultures and further augmented hypoxic injury in these neurons; 3) DOR activation ([D-Ala2,D-Leu5]enkephalin) reduced neuronal injury in day 8 cultures after 24 h of normoxic or hypoxic exposure and attenuated naltrindole-induced injury with prolonged exposure; and 4) µ- or kappa -opioid receptor inhibition (beta -funaltrexamine or nor-binaltorphimine) had little effect on neurons in either normoxic or hypoxic conditions. Collectively, these data suggest that DOR plays a crucial role in neuroprotection in normoxic and hypoxic environments.

cortex; hypoxia; injury; protection; opioids

* J. Zhang and G. T. Gibney contributed equally to this work.




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