Interrupting the trigeminal pathway centrally or peripherally
eliminates the cardiac response to simulated diving.
McCulloch, P. F., I. A. Paterson, and N. H. West.
Departments of Physiology and Psychiatry, and Neuropsychiatric
Research Unit, College of Medicine, University of Saskatchewan,
Saskatoon, Saskatchewan, S7N 0W0, CANADA
APStracts 2:0101R, 1995.
Nasal water flow plus concomitant expiratory apnea in anesthetized
(Innovar-Vet), paralyzed and artificially ventilated rats produce
immediate bradycardia. To investigate the origin of this response,
four procedures were used to block the trigeminal pathway. 1)
Trigeminal receptors within the nasal passages were anesthetized by
infusing local anesthetic through the external nares. 2) Trigeminal
nerves that innervate the nasal passages were sectioned bilaterally
as they passed through the orbit. 3) The trigeminal neural pathway
was blocked within the brain stem, by either electrolytically
lesioning or infusing local anesthetic into the spinal trigeminal
nucleus interpolaris (Sp5I). 4) Synaptic transmission within Sp5I was
prevented by infusing glutamate receptor antagonists AP-7 and DNQX.
After completion of each of the procedures, the cardiovascular
responses to nasal water flow plus apnea were either attenuated or
eliminated. The major conclusion of this study is that an intact
glutamatergic trigeminal pathway is required for manifestation of the
cardiovascular responses to nasal stimulation. Evidence also suggests
that NMDA and non-NMDA glutamate receptors are both required for
synaptic neurotransmission within Sp5I.
Received 19 December 1994; accepted in final form 3 April 1995.
APS Manuscript Number R718-4.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 April 1995.