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Regulation of ventral surface chemoreceptors by purinergic signaling
Author(s) -
Wenker Ian Christopher,
Takakura Ana,
Moreira Thiago,
Mulkey Daniel Kent
Publication year - 2012
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.26.1_supplement.894.1
Subject(s) - chemoreceptor , purinergic receptor , carbenoxolone , gap junction , bursting , neuroscience , extracellular , brainstem , electrophysiology , biology , chemistry , receptor , microbiology and biotechnology , biochemistry , intracellular
A brainstem region called the retrotrapezoid nucleus (RTN) contains a population of CO 2 /H + ‐sensitive neurons that appear to function as important central chemoreceptors (i.e. CO 2 /H + sensors). Evidence also indicates that CO 2 /H + ‐evoked ATP release contributes to RTN chemoreception. The goals of this study are to determine the extent to which ATP contributes to RTN chemoreception both in vivo and in vitro, and determine whether purinergic drive to chemoreceptors relies on extracellular Ca 2+ or gap junction hemichannels. In vivo , phrenic nerve recordings of respiratory activity in adult rats show that bilateral injection of P2‐ receptor antagonists decreased the ventilatory response to CO 2 by 30%. Likewise, in vitro , recordings from functionally identified RTN chemoreceptor neurons in brainstem slices from rat pups (p7–p12), we show P2‐receptor antagonists decreased the firing rate response of RTN neurons to CO 2 also by 30%. In the slice, this purinergic drive to breathe did not increase with temperature and was retained in low [Ca 2+ ]o. Conversely, gap junction blockers carbenoxolone (100 μM) and cobalt (500 μM) decreased neuronal CO 2 /H + ‐sensitivity by an amount similar to P2‐receptor antagonists. These results support the possibility that astrocytes but not neurons mediate CO 2 /H + ‐evoked ATP release possibly by a mechanism involving gap junction hemichannels.