Electrophysiological properties of rostral ventrolateral medulla presympathetic neurons modulated by the respiratory network in rats.

Moraes DJ, da Silva MP, Bonagamba LG, Mecawi AS, Zoccal DB, Antunes-Rodrigues J, Varanda WA, Machado BH. J Neurosci. 2013 Dec 4;33(49):19223-37 In this paper, they looked at presympathetic cells and how some of them are modulated by respiratory activity. They started by looking at rats that had been exposed to chronic intermittent hpoxia (CIH) and found that CIH caused increases in arterial pressure, abdominal electromyography, and abdominal and thoracic nerve activity. They next used whole cell blind patch clamp in the working rat heart-brainstem preparation. They identified presympathetic neurons by position, inhibiinhibitory response to baroreflex, and antidromic action potentials caused by electrical stimuli at T8-12. What they found was that presympathetic neurons were "noisy," which means that that, in addition to spontaneous APs, there were many transient changes in membrane potential that were related to respiration, seemingly due to EPSPs. They identified 4 different groups of presympathetic neurons - (1) Neurons with very regular discharge that were not modulated by respiratory activity, (2) irregular neurons with inspiratory modulation, (3) irregular neurons with post-inspiratory modulation, and (4) regular with inspiratory inhibition. Their results were pretty interesting in that all the C1 neurons they identified (by post-test immuno and single cell qRT-PCR using the cytoplasm which was aspirated after patch recording) fell in to groups 1 and 2, but were NOT different between normal and CIH groups. Group 4 consisted of non-C1 neurons that did not differ between groups. Group 3, however, consisted of non-C1 neurons that WERE different between groups. Apparently, CIH causes some non-c1 presympathetic neurons to fire faster in a way that is NOT due to any changes in their own membrane properties (spikes per current injection, input resistance), but rather through changes in their input (Dare we say that it might be due to changes in their sensitivity to excitatory input?) Anyway, they found evidence that some of the changes may be due to differences in pacemaker current activity, which seemed to be due to INaP, which is a persistent inactivating sodium current. This TTX-sensitive current is known to generate subthreshold oscillations in membrane potential, which can change neuronal excitability. So I guess the moral of this story is that if you can't exercise, make sure you get plenty of oxygen all the time, or else you're in serious trouble. -DH