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Delta‐opioid receptor (DOR) activation is neuroprotective during oxygen‐glucose deprivation (OGD) in neonatal rat medullary slices in vitro
Author(s) -
Majewski David J.,
Johnson Stephen M.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1233.4
Subject(s) - neuroprotection , agonist , anesthesia , neuroscience , respiratory system , rhythm , chemistry , receptor , biology , pharmacology , medicine
OGD can cause long‐lasting damage to the CNS and cell death. DOR activation prior to OGD is neuroprotective in cardiac tissue, but it is not known whether DOR activation protects oscillatory motor networks, such as the respiratory rhythm generator. To address this question, respiratory‐related hypoglossal (XII) motor bursts were recorded with suction electrodes from rhythmically active neonatal rat (P0–P3) medullary slices. Application of OGD solution (oxygen‐ and glucose‐free) decreased spontaneous respiratory burst amplitude by 53 ± 5% within 10 min and bursts were abolished within 21.6 ± 1.5 min (n = 5). In contrast, application of DPDPE (1.0 μM; DOR agonist) for 10 min prior to and during OGD solution application caused XII burst amplitude to decrease by only 24 ± 5% at 10 min and bursts were abolished at 31.4 ± 3.9 min (n = 5; p < 0.01 for drug effect). OGD‐induced changes in burst frequency were nearly identical during OGD solution application alone or with DPDPE co‐application. These data suggest that XII motoneurons are more vulnerable to OGD than rhythm‐generating neurons, and that DOR activation is neuroprotective during OGD in oscillatory motor networks.