Cortical δ-Opioid Receptors Potentiate K+ Homeostasis During Anoxia and Oxygen–Glucose Deprivation

• DOI: 10.1038/sj.jcbfm.9600352
• Publication Date: 2006-06-14T11:54:41Z
• Authors: Dongman Chao; David F Donnelly; Yin Feng; Alia Bazzy-Asaad; Ying Xia
• Keywords: Naltrindole; Homeostasis; Chelerythrine

Central neurons are extremely vulnerable to hypoxic/ischemic insult, which is a major cause of neurologic morbidity and mortality as consequence neuronal dysfunction death. Our recent work has shown that δ-opioid receptor (DOR) neuroprotective against hypoxic excitotoxic stress, although the underlying mechanisms remain unclear. Because hypoxia/ischemia disrupts ionic homeostasis with an increase in extracellular K + , plays role death, we asked whether DOR activation preserves during stress. To test this hypothesis, recordings -sensitive microelectrodes were performed mouse cortical slices under anoxia or oxygen–glucose deprivation (OGD). The main findings study (1) [D-Ala 2 D-Leu 5 ]-enkephalinamide attenuated anoxia- OGD-induced decrease DC potential slices; (2) inhibition naltrindole, antagonist, completely abolished DOR-mediated prevention potential; (3) protein kinase A (PKA) N-(2-[p-bromocinnamylamino]-ethyl)-5-isoquinolinesulfonamide dihydrochloride had no effect on protection; (4) C (PKC) chelerythrine chloride reduced protection, whereas PKC activator (phorbol 12-myristate 13-acetate) mimicked homeostasis. These data suggest protects cortex ODG-induced derangement potassium homeostasis, protection occurs via PKC-dependent PKA-independent pathway. We conclude important aspect neuroprotection its early action ischemia.