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Sustained apnea induced by GABAA receptor blockade at ventrolateral pons/A5 region is reversed by subsequent blockade of glutamatergic receptors
Author(s) -
Song Gang,
Ning Yinghui,
Poon ChiSang
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.931.5
Subject(s) - pons , bicuculline , glutamatergic , gabaa receptor , blockade , anesthesia , neuroscience , cnqx , excitatory postsynaptic potential , medicine , chemistry , inhibitory postsynaptic potential , endocrinology , glutamate receptor , receptor , biology , ampa receptor
The A5 region in ventrolateral pons (vl‐pons/A5) is thought to be an auxiliary substrate for the putative pneumotaxic center in the dorsolateral pons that modulates inspiratory‐expiratory phase switching (inspiratory off‐switch), post‐inspiratory activity (post‐I) and expiratory duration (TE). In urethane‐anesthetized, vagotomized and ventilated adult SD rats, we observed that blockade of GABAA receptors at vl‐pons/A5 by unilateral microinjection of bicuculline (BIC) caused prolongation of vagal post‐I motor activity and TE, an effect that was similar to that evoked by electrical or chemical stimulations in this region. Bilateral microinjections of BIC caused further protracted prolongation of TE or even sustained apnea with complete cessation of phrenic activity and prolongation of post‐I activity. Remarkably, the apnea so induced was reversed and rhythmic phrenic discharges gradually resumed upon subsequent blockade of excitatory glutamatergic receptors by bilateral microinjections of CNQX and AP‐5 at the same vl‐pons/A5 sites, or by the application of hypoxic or hypercapnic stimuli. These findings indicated that the vl‐pons/A5 plays an important role in promoting post‐I activity and inspiratory off‐switch subject to a delicate balance between GABAA receptor‐mediated inhibitory and glutamatergic receptor‐mediated excitatory modulations. (Supported by HL093225)