Changes in Opioid and Ach of the Rat Brain during Resistive Loaded Breathing

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(1) We have examined changes of mRNA for preproenkephaline (PPE)-A, which is a precursor of enkephaline, in the rats cerebral cortex during chronic resistive loaded breathing. Northern blot revealed that PPE-A mRNA was induced after 3 days of airway stenosis, and the induction continued for at least 2 weeks. In situ hybridization revealed that PPE-A was gradually induced in frontal cortex. These results suggest that the endogenous opioid system may be at work as an important compensatory mechanism to reduce the reaspiratory sensation during chronic respiratory stress.(2) We have investigated acetylcholine (Ach) release in the hypocampus, cingulate cortex or hypothalamus of rat brain during hypercapnia or hypoxia. 10% CO_2 induced Ach in the hypocampus and hypothalamus by 30-100%, but it did not induced in the striatum. Hypoxia increased Ach in the same area, but the degree was much smaller than that of hypercapnia.(3) We measured glutamate (Glu) release in the nucleus tractus solitarius of rats brain during hypoxia by using in vivo microdialysis. Glutamate increased during hypoxia or during doxapram infusion in carotid body intact rats, but it did not increased in rats with bilateral carotid body resection. Microinjected glutamate into the NTS increased ventilation. MK801, a NMDA receptor antagonist, perfused in the NTS blocked the ventilatory increase during hypoxic ecposure. These results suggests that glutamate may be a neurotransmitter in the NTS in response to peripheral chemoreceptor activation during hypoxia.