Intrinsic properties of rostral ventrolateral medulla presympathetic and bulbospinal respiratory neurons of juvenile rats are not affected by chronic intermittent hypoxia.

The presympathetic neurons in the rostral ventrolateral medulla (RVLM) are considered to be the source of the sympathetic activity, and there is experimental evidence that these cells present intrinsic autodepolarization. There is also evidence that an important respiratory neuronal population located in the RVLM/Bötzinger complex (BötC) corresponds to augmenting expiratory neurons (aug-E), which send projections to the phrenic nucleus in the spinal cord. However, the pacemaker activity of presympathetic neurons and the intrinsic properties of aug-E neurons had not been evaluated in brainstem slices of juvenile rats (postnatal day 35). Chronic intermittent hypoxia (CIH) is a sympathetic-mediated hypertension model, which seems to produce an associated increase in the activity of aug-E neurons. In this study, we evaluated the effects of CIH on the intrinsic properties of RVLM/BötC presympathetic and phrenic nucleus-projecting neurons (aug-E) in brainstem slices of juvenile rats (postnatal day 35). We observed that all presympathetic neurons presented spontaneous action potential firing (n = 18), which was not abolished by ionotropic receptor antagonism. In addition, exposure to 10 days of CIH produced no changes in their intrinsic passive properties, firing pattern or excitability. Most aug-E neurons presented spontaneous firing in control conditions (13 of 15 neurons), and this characteristic was preserved after blocking fast synaptic transmission (12 of 15 neurons), clearly demonstrating their intrinsic pacemaker activity. Chronic intermittent hypoxia also produced no changes in intrinsic passive properties, frequency and pattern of discharge or excitability of the aug-E neurons. The present study shows that: (i) it is possible to record the electrophysiological properties of RVLM/BötC presympathetic and aug-E neurons in brainstem slices from juvenile rats; (ii) these neurons present characteristics of intrinsic pacemakers; and (iii) their intrinsic properties were not altered by chronic intermittent hypoxia.