NMDA RECEPTOR-MEDIATED TRANSMISSION OF CAROTID-BODY CHEMORECEPTOR INPUT TO EXPIRATORY BULBOSPINAL NEURONS IN DOGS
NMDA RECEPTOR-MEDIATED TRANSMISSION OF CAROTID-BODY CHEMORECEPTOR INPUT TO EXPIRATORY BULBOSPINAL NEURONS IN DOGS
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DOI：
10.1113/jphysiol.1995.sp020906
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发表时间：
1995-09-15
影响因子：
5.5
通讯作者：
ZUPERKU, EJ
中科院分区：
文献类型：
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作者：
DOGAS, Z;STUTH, EAE;ZUPERKU, EJ
1.本研究验证了兴奋性氨基酸受体介导呼气球脊髓神经元对颈动脉体化学感受器输入的兴奋性反应的假说.研究仅在硫喷妥钠麻醉、麻痹、通气、迷走神经切断的狗中进行。快速、短时间化学感受器激活是通过向自体灌注的颈动脉中双侧推注CO2饱和盐水（P-CO2 > 700 mmHg）产生的。加压储液器电磁阀系统用于在神经呼气相开始之前输送CO2推注，如从膈神经图确定的，大约每分钟一次。多管微量移液器仅用于记录神经元单位活动和传递神经递质。呼气球脊髓神经元对外周化学感受器激活的净反应通过从CO2测试团给药期间的F-n中减去三个控制呼气周期期间的平均放电频率（F-n）来确定。通过比较NMDA受体拮抗剂2-amino-5-phosphonovalerate（AP 5）或非NMDA受体拮抗剂2，3-dihydroxy-6-硝基-7-sulphamoyl-benzo（f）quinoxaline（NBQX）压力微喷射之前、期间和之后的基线和团注呼气神经元F-n来确定兴奋性氨基酸受体在介导这种反应中的作用。通过监测移液器尖端的运动来测量AP 5和NBQX的喷射率. AP 5在对照和大剂量周期期间均降低了F-n，并降低了对照和大剂量周期之间的F-n变化。NBQX对基线或推注反应均无影响。AP 5不能阻止AMPA对呼气泡脊髓神经元的兴奋。AMPA与AP 5联合给药可阻止AP 5介导的F-n降低，但不能阻止CO2推注反应的剂量依赖性降低。两者合计，这些数据强烈表明，颈动脉化学受体介导的呼气球脊髓神经元的兴奋依赖于NMDA，但不是非NMDA谷氨酸受体。
1. This study tested the hypothesis that excitatory amino acid receptors mediate the excitatory response of expiratory bulbospinal neurones to carotid body chemoreceptor inputs.2. Studies mere carried out in thiopental sodium anaesthetized, paralysed, ventilated, vagotomized dogs.3. Brisk, short-duration chemoreceptor activation nas produced by bilateral bolus injections of CO2-saturated saline (P-Co2 > 700 mmHg) into the autoperfused carotid arteries. A pressurized-reservoir-solenoid valve system was used to deliver the CO2 bolus injections just prior to the onset of the neural expiratory phase, as determined from the phrenic neurogram, about once per minute.4. Multibarrelled micropipettes mere used to record neuronal unit activity and deliver neurotransmitter agents. Net responses of expiratory bulbospinal neurones to peripheral chemoreceptor activation were determined by subtracting the mean discharge frequencies (F-n) during three control expiratory cycles from the F-n during administration of a CO2 test bolus. The role of excitatory amino acid receptors in mediating this response was determined by comparing the baseline and bolus expiratory neuronal F-n before, during and after the pressure microejection of the NMDA receptor antagonist 2-amino-5-phosphonovalerate (AP5) or the non-NMDA receptor antagonist 2,3-dihydroxy-6-nitro-7-sulphamoyl-benzo(f)quinoxaline (NBQX). Ejection rates of AP5 and NBQX were measured by monitoring the movement of the pipette meniscus.5. AP5 reduced F-n during both the control and bolus cycles, as well as reducing the change in F-n between control and bolus cycles. NBQX had no effect on either baseline or bolus responses.6. AP5 did not prevent excitation of expiratory bullospinal neurones by AMPA. Coadministration of AMPA with AP5 prevented the AP5-mediated decrease in F-n but not the dose-dependent reduction in the CO2 bolus response.7. Taken together, these data strongly suggest that the carotid chemoreceptor-mediated excitation of expiratory bulbospinal neurones is dependent on NMDA but not non-NMDA glutamate receptors.