N-methyl-D-aspartate receptors mediate chemoreflexes in the shorthorn sculpin Myoxocephalus scorpius.

Glutamate microinjected into the vagal sensory area in the medulla produces cardiorespiratory responses mimicking oxygen chemoreflexes in fish. Here we directly investigate whether these reflexes are dependent on the ionotropic N-methyl-D-aspartate (NMDA) glutamate receptor. Fish were equipped with opercular, branchial and snout cannulae for measurements of cardiorespiratory parameters and drug injections. Oxygen chemoreceptor reflexes were evoked by rapid hypoxia, NaCN added into the blood (internal, 0.3 ml, 50 microg ml(-1)) and the mouth (external, 0.5 ml, 1 mg ml(-1)), before and after systemic administration of the NMDA receptor antagonist MK801 (3 mg kg(-1)). Hypoxia produced an MK801-sensitive increase in blood pressure and ventilation frequency, whereas the marked bradycardia and the increased ventilation amplitude were NMDA receptor-independent. The fish appeared more responsive to externally applied cyanide, but the injections and MK801 treatment did not distinguish whether external or internal oxygen receptors were differently involved in the hypoxic responses. In addition, using single-labelling immunohistochemistry on sections from the medulla and ganglion nodosum, the presence of glutamate and NMDA receptors in the vagal oxygen chemoreceptor pathway was established. In conclusion, these results suggest that NMDA receptors are putative central control mechanisms that process oxygen chemoreceptor information in fish.