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Effects of IV remifentanil (Remi) on the discharge of canine pontine respiratory group (PRG) neurons in the parabrachial complex (PB)

Mu‐opioids at clinical doses produce bradypnea, which is reversed by microinjection of naloxone into the pontine PB. We studied the effects of the mu‐opioid agonist Remi (IV) on PRG neuron discharge patterns in decerebrate, vagotomized, ventilated, paralyzed dogs. A NeuroNexus 16‐electrode microprobe was used to record from multiple PRG neurons before, during and after IV Remi. Histograms (CTHs) of PRG discharge patterns, triggered from the phrenic neurogram (PNG), were used to quantify Remi effects on ten PRG neuron subtypes. Remi (0.5–0.8 mcg/kg/min) increased TI and TE by 21% and 23% respectively, and decreased peak PNG by 33±3%. PRG neurons (n=197) were located 0.5–2 mm caudal to inferior colliculus, 5–6.5 mm lateral to midline and 2.5–4.5 mm below the dorsal surface. The depression (peak Fn) of all PRG neurons (28±3%; n=197) was similar among 9 of 10 subtypes, but Edec neurons were more depressed (70±6%; n=24; p<0.001). Magnitude of neuronal depression was not related to control Fn, or changes in TI or TE except for Icon neurons and TI (r = −0.72; p<0.001). PRG neurons, except Edec, were less depressed than the peak PNG. Marked depression in PRG Edec neurons may underlie loss of recurrent laryngeal Edec activity. Opioid‐induced depression of PRG subtypes coincident with bradypnea is consistent with reduced excitation to medullary rhythm generation. Supported by VA Merit Review Award: 1 I01 BX000721–01.