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Accelerators and brakes in CO 2 chemosensitive neurons
Author(s) -
Quintero Maria Carolina,
Cordovez Juan Manuel,
Putnam Robert W.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1137.25
Subject(s) - neuronal firing , chemistry , locus coeruleus , neuron , neuroscience , biophysics , electrophysiology , biology , central nervous system
The cellular factors that determine the magnitude of the firing rate response of chemosensitive neurons to increased CO 2 /H + are typically attributed to acid‐induced increased firing rate pathways (accelerators). However, a marked reduction in the CO 2 /H + ‐induced increased firing rate during postnatal development has been observed in neurons from the locus coeruleus (LC). This response has been hypothesized to be due to the development of a decelerating pathway that arises from CO 2 /H + activation of Ca 2+ channels, which in turn induces the Ca 2+ ‐activation of K Ca channels. In order to investigate the contribution of such a braking pathway in the magnitude of the firing rate in individual neurons, we have developed a preliminary computational model of excitable single neuron that simulates the voltage‐gated currents as well as the pH and Ca 2+ sensitive K + currents using the Hodgkin‐Huxley formulation. In our simulations we found that inhibition of the L‐type Ca 2+ current led to a larger hypercapnic‐induced firing rate response. These findings constitutes theoretical evidence that the cellular factors limiting the firing rate response of chemosensitive neurons are associated with acid activated Ca 2+ and Ca 2+ activated K Ca currents, allowing us to conclude that a braking pathway may play a more significant role in setting neuronal chemosensitivity. Supported by NIH Grant HL56683.