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Hypothalamic disinhibition stimulates retrotrapezoid nucleus (RTN) chemosensitive neurons in vivo
Author(s) -
Fortuna Michal G,
Stornetta Ruth L,
West Gavin H,
Guyenet Patrice G
Publication year - 2009
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.23.1_supplement.946.2
Subject(s) - stimulation , inhibitory postsynaptic potential , excitatory postsynaptic potential , neuroscience , chemistry , respiratory center , premovement neuronal activity , respiratory system , medicine , biology
Stimulation of neurons within the dorsomedial hypothalamic nucleus (DMH) and perifornical area (PeF) produces an increase of respiratory activity, tachycardia and a marked pressor response. The descending pathway mediating the respiratory arm of this complex response is not well characterized. Intrinsically pH sensitive retrotrapezoid nucleus (RTN) neurons are proposed to produce excitatory drive to the respiratory network (CPG). We sought to determine if pharmacological stimulation of DMH/PeF would result in an increased activity of RTN neurons, and to determine if this response is dependent on the CPG. RTN unit activity was monitored in adult, isoflurane‐anesthetized rats. Here we report that stimulation of DMH/PeF with the selective GABAA antagonist, gabazine, increases phrenic nerve activity (PNA) as previously reported and markedly increases the discharge rate of RTN units. This effect was independent of the CO2 level and respiratory modulation of the RTN cells in general was not affected. Moreover after silencing the CPG with morphine, hypothalamic stimulation was still able to increase RTN activity, even before the CPG was reactivated. Morphine also had a mild inhibitory effect on the RTN neurons. In summary we propose that the descending pathway from DMH/PeF that activates respiration might be in part mediated through RTN chemosensitive neurons.