AN INTACT GLUTAMATERGIC TRIGEMINAL PATHWAY IS ESSENTIAL FOR THE CARDIAC RESPONSE TO SIMULATED DIVING

Nasal water flow plus concomitant expiratory apnea in anesthetized (In novar-Vet), paralyzed, and artificially ventilated rats produces immed iate bradycardia. To investigate the origin of this response, four pro cedures were used to block the trigeminal pathway. 1) Trigeminal recep tors within the nasal passages were anesthetized by infusing local ane sthetic through the external nares. 2) Trigeminal nerves that innervat e the nasal passages were sectioned bilaterally as they passed through the orbit. 3) The trigeminal neural pathway was blocked within the br ain stem by either electrolytically lesioning or infusing local anesth etic into the spinal trigeminal nucleus interpolaris (Sp5I). 4) Synapt ic transmission within Sp5I was prevented by infusing glutamate recept or antagonists D-2-amino-7-phosphonoheptanoic acid and 6,7-dinitroquin oxaline-2,3-dione. After each of the procedures was completed, the car diovascular responses to nasal water flow plus apnea were either atten uated or eliminated. The major conclusion of this study is that an int act glutamatergic trigeminal pathway is required for manifestation of the cardiovascular responses to nasal stimulation. Evidence also sugge sts that N-methyl-Daspartate (NMDA) and non-NMDA glutamate receptors a re both required for synaptic neurotransmission within Sp5I.