Abstract
Ischemic-hypoxic neuro-excitation and toxicity have been attributed to a rapid release of glutamate and formation of nitric oxide. We have now demonstrated that sympatho-excitatory response (1.2-fold increase in sympathetic nerve activity) induced by intratracheal administration of 100% N 2 for 20 s in anesthetized rats and membrane inward currents (0.4–0.5 nA) induced by cyanide (300 μM) and hypoxia (saturated with 75% N 2) of these neurons recorded in slices of rat rostral ventrolateral medulla were neither reduced by blocking glutamate receptors with kynurenate, synaptic transmission with tetrodotoxin nor by inhibiting nitric oxide synthase with N- nitro- l-arginine , indicating that glutamate, synaptic inputs, and nitric oxide are not involved in rapid responses of reticulospinal vasomotor neurons to hypoxia.
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