Open AccessA direct excitatory action of lactate ions in the central respiratory network
Author(s) -
Michael T. Burton,
Joseph M. Santin
Publication year - 2020
Publication title -
journal of experimental biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.367
H-Index - 185
eISSN - 1477-9145
pISSN - 0022-0949
DOI - 10.1242/jeb.235705
Subject(s) - excitatory postsynaptic potential , chemoreceptor , control of respiration , brainstem , neuroscience , ventilation (architecture) , respiratory system , biology , postsynaptic potential , inhibitory postsynaptic potential , chemistry , medicine , biophysics , biochemistry , anatomy , receptor , mechanical engineering , engineering
Chemoreceptors that detect O2 and CO2/pH regulate ventilation. However, recent work shows that lactate ions activate arterial chemoreceptors independent of pH to stimulate breathing. Although lactate rises in the central nervous system (CNS) during metabolic challenges, the ability for lactate ions to enhance ventilation by directly targeting the central respiratory network remains unclear. To address this possibility, we isolated the amphibian brainstem-spinal cord and found that small increases in CNS lactate stimulate motor output that causes breathing. In addition, lactate potentiated the excitatory postsynaptic strength of respiratory motor neurons, thereby coupling central lactate to the excitatory drive of neurons that trigger muscle contraction. Lactate did not affect motor output through pH or pyruvate metabolism, arguing for sensitivity to lactate anions per se. In sum, these results introduce a mechanism whereby lactate ions in the CNS match respiratory motor output to metabolic demands.