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First published online October 17, 2008
Journal of Experimental Biology 211, 3512-3517 (2008)
Published by The Company of Biologists 2008
doi: 10.1242/jeb.021949
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{delta}-Opioid receptor antagonism induces NMDA receptor-dependent excitotoxicity in anoxic turtle cortex

Matthew E. Pamenter1 and Leslie T. Buck2,3,*

1 Department of Pediatrics and Neuroscience, University of California San Diego, La Jolla, CA 92093, USA
2 Department of Cellular and Systems Biology, University of Toronto, Toronto, ON, Canada, M5S 3G5
3 Department of Ecology and Evolutionary Biology, University of Toronto, Toronto, ON, Canada, M5S 3G5


Figure 1
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  		Fig. 1. Neuronal responses to naltrindole during anoxia. For each panel the top trace (membrane potential, Em) and the middle trace (change in cytosolic [Ca2+], {Delta}[Ca2+]c) correspond to the same treatment regime, as indicated by the solid black bars. The whole-cell NMDAR currents (bottom trace) were recorded at the time points indicated by a, b or c on the Em trace within the same panel. All experiments were conducted on individual cortical sheets exposed to (A) normoxia, (B) anoxia, (C) normoxia plus naltrindole, (D) anoxia plus naltrindole, (E) anoxia plus naltrindole in the presence of the NMDAR antagonist 2-amino-5-phosphonopentanoic acid (APV), or (F) anoxia plus naltrindole in the presence of the Gi agonist mastoparan-7 (MP7).

 

Figure 2
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  		Fig. 2. Naltrindole enhances anoxic neuronal depolarization via Gi protein inhibition. Summary of Em changes from cortical neurons during treatment. Em was assessed as the mean of sequential 5 min recording segments. Data are expressed as means ± s.e.m. *Data significantly different from normoxic controls; {dagger}data significantly different from anoxic controls. Significance was assessed at P<0.05. The bar indicates the duration of the treatment indicated in the key.

 

Figure 3
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  		Fig. 3. Naltrindole potentiates normoxic NMDAR currents and reverses the anoxic decrease in NMDAR currents via Gi protein inhibition. Summary of changes in NMDAR currents during treatment. Data are expressed as means ± s.e.m. *Data significantly different from normoxic controls; {dagger}data significantly different from anoxic controls; {ddagger}data significantly different from anoxic neurons treated with naltrindole. Significance was assessed at P<0.05. The bar indicates the duration of the treatment indicated in the key.

 

Figure 4
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  		Fig. 4. Naltrindole induces severe NMDAR-mediated calcium influx. Summary of changes in [Ca2+]c during normoxia and anoxia with and without the {delta}-opiod receptor (DOR) antagonist naltrindole alone or in the presence of APV or MP7. Data are expressed as means ± s.e.m. *Data significantly different from normoxic control; {dagger}data significantly different from anoxic control; {ddagger}data significantly different from anoxia plus naltrindole treatment. Significance was assessed at P<0.05.

 

Figure 5
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  		Fig. 5. NMDAR blockade abolishes excitatory events in anoxia plus naltrindole-treated neurons. Seizure-like events induced by perfusion of naltrindole during anoxia were abolished by co-perfusion of the NMDAR antagonist APV, preventing further anoxic depolarization and excitotoxic cell death.

 

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