Journal
NEURON
Volume 34, Issue 5, Pages 821-830Publisher
CELL PRESS
DOI: 10.1016/S0896-6273(02)00712-2
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Funding
- NHLBI NIH HHS [R01 HL040959, HL-40959] Funding Source: Medline
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We tested the hypothesis that pacemaker neurons generate breathing rhythm in mammals. We monitored respiratory-related motor nerve rhythm in neonatal rodent slice preparations. Blockade of the persistent sodium current (I(NaP)), which was postulated to underlie voltage-dependent bursting in respiratory pacemaker neurons, with riluzole (less than or equal to200 muM) did not alter the frequency of respiratory-related motor output. Yet, in every pacemaker neuron recorded (50/50), bursting was abolished at much lower concentrations of riluzole (less than or equal to520 muM). Thus, eliminating the pacemaker population (our statistics confirm that this population is reduced at least 94%, p < 0.05) does not affect respiratory rhythm. These results suggest that voltage-dependent bursting in pacemaker neurons is not essential for respiratory rhythmogenesis, which may instead be an emergent network property.
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