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Constance S. Kaufman Pediatric Pulmonary Research Laboratory, Departments of Pediatrics and Physiology, Tulane University School of Medicine, and Department of Cardiopulmonary Science, Louisiana State University School of Allied Health, New Orleans, Louisiana 70112
This study aimed
to determine the role of protein kinase C (PKC) in signal transduction
mechanisms underlying ventilatory regulation in the nucleus tractus
solitarii (NTS). Microinjection of phorbol 12-myristate 13-acetate into
the commissural NTS of nine chronically instrumented, unrestrained rats
elicited significant cardiorespiratory enhancements that lasted for at
least 4 h, whereas administration of vehicle
(n = 15) or the inactive phorbol ester 4
-phorbol 12,13-didecanoate (n = 7)
did not elicit minute ventilation (
E)
changes. Peak hypoxic E
responses (10% O2-balance
N2) were measured in 19 additional animals after NTS microinjection of bisindolylmaleimide
(BIM) I, a selective PKC inhibitor (n = 12), BIM V (inactive analog; n = 7),
or vehicle (Con; n = 19). In Con,
E increased from 139 ± 9 to 285 ± 26 ml/min in room air and hypoxia, respectively, and similar
responses occurred after BIM V. BIM I did not affect room air
E but markedly attenuated hypoxia-induced E increases (128 ± 12 to 167 ± 18 ml/min; P < 0.02 vs. Con and BIM V). When BIM I was microinjected into the cerebellum
(n = 4), cortex
(n = 4), or spinal cord
(n = 4),
E responses were similar to Con.
Western blots of subcellular fractions of dorsocaudal brain stem
lysates revealed translocation of PKC, 
, 
, 
, 
, and 
isoenzymes during acute hypoxia, and enhanced overall PKC activity was
confirmed in the particulate fraction of dorsocaudal brain stem lysates
harvested after acute hypoxia. These studies suggest that, in the adult
rat, PKC activation in the NTS mediates essential components of the
acute hypoxic ventilatory response.
brain stem; signal transduction; respiratory control
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