The identity and location of central pH/CO2 sensitive chemoreceptors are not fully
understood. Serotonin (5-HT) and γ-aminobutyric acid (GABA) synthesizing neurons in the medullary raphé have demonstrated intrinsic chemosensitivity in vitro. This
evidence forms the basis for our "push-pull" model of raphé contributions to chemosensitivity. We have previously shown that CO2-stimulated 5-HT neurons occur
in the medullary raphé in situ. Here, we test the hypothesis that the medullary raphé
contains GABA synthesizing CO2-inhibited neurons that retain their chemosensitivity
after pharmacological blockade of major fast synaptic inputs. To assess chemosensitivity, we record extracellular single neuron discharge during normocapnic and hypercapnic conditions within the medullary raphé of the unanesthetized juvenile rat in situ perfused decerebrate brainstem preparation. Network dependence of chemosensitivity is assessed by application of antagonists for AMPA, NMDA, glycine, and GABAa receptors that disrupt fast-synaptic network properties. Juxtacellular labeling and immunohistochemistry establish neurotransmitter phenotypes of recorded
neurons. Results support independence of CO2-inhibited GABA neuron chemosensitivity from fast synaptic inputs.Supported by NIH 54NS041069-06A1
