Abstract
Findings in newborn mouse brainstem slices led to the hypothesis that depression of breathing by opioids is caused by postsynaptic K(+) channel-mediated hyperpolarization of rhythmogenic inspiratory neurons of the pre-Bötzinger complex (preBötC). Subsequent observations in newborn en bloc medullas and juvenile rats in vivo indicated that excitatory drive from retrotrapezoid nucleus/parafacial respiratory group (RTN/pFRG) neurons partly counters opioid-evoked inspiratory inhibition. Our recent study in newborn rat en bloc medullas supports the latter hypothesis, whereas we found in that report that inspiratory preBötC neurons constituting the interface with the RTN/pFRG are not hyperpolarized by opioids. Here, we show that opioids also do not hyperpolarize preBötC neurons in "calibrated" newborn rat slices. This supports the previous hypothesis by us and others that opioids rather target inspiratory networks indirectly, likely primarily via presynaptic mechanisms.
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