生理学报
生理學報
생이학보
ACTA PHYSIOLOGICA SINICA
2001年
2期
89-92
,共4页
非NMDA受体%双相呼气神经元%吸气神经元%放电频率%峰频率%突触输入
非NMDA受體%雙相呼氣神經元%吸氣神經元%放電頻率%峰頻率%突觸輸入
비NMDA수체%쌍상호기신경원%흡기신경원%방전빈솔%봉빈솔%돌촉수입
在新生大鼠延髓脑片上同步记录舌下神经根和双相呼气神经元/吸气神经元单位的放电活动, 并在灌流的改良Kreb′s液中先后加以非NMDA受体的激动剂KA和拮抗剂DNQX, 观察对神经元单位放电的影响, 以进一步探讨非NMDA受体在对双相呼气神经元之间交互兴奋和吸气神经元兴奋性突触输入中的作用。结果表明, 使用非NMDA受体激动剂KA以后, 双相呼气神经元的放电频率和峰频率都明显增大, 吸气神经元中期放电的频率和峰频率也显著增大, 而早期和晚期放电的频率无明显改变; 用相应拮抗剂以后, 上述效应明显被抑制。结果提示, 非NMDA受体参与了双相呼气神经元之间的交互兴奋作用, 并且也介导了吸气神经元的兴奋性突触输入。
在新生大鼠延髓腦片上同步記錄舌下神經根和雙相呼氣神經元/吸氣神經元單位的放電活動, 併在灌流的改良Kreb′s液中先後加以非NMDA受體的激動劑KA和拮抗劑DNQX, 觀察對神經元單位放電的影響, 以進一步探討非NMDA受體在對雙相呼氣神經元之間交互興奮和吸氣神經元興奮性突觸輸入中的作用。結果錶明, 使用非NMDA受體激動劑KA以後, 雙相呼氣神經元的放電頻率和峰頻率都明顯增大, 吸氣神經元中期放電的頻率和峰頻率也顯著增大, 而早期和晚期放電的頻率無明顯改變; 用相應拮抗劑以後, 上述效應明顯被抑製。結果提示, 非NMDA受體參與瞭雙相呼氣神經元之間的交互興奮作用, 併且也介導瞭吸氣神經元的興奮性突觸輸入。
재신생대서연수뇌편상동보기록설하신경근화쌍상호기신경원/흡기신경원단위적방전활동, 병재관류적개량Kreb′s액중선후가이비NMDA수체적격동제KA화길항제DNQX, 관찰대신경원단위방전적영향, 이진일보탐토비NMDA수체재대쌍상호기신경원지간교호흥강화흡기신경원흥강성돌촉수입중적작용。결과표명, 사용비NMDA수체격동제KA이후, 쌍상호기신경원적방전빈솔화봉빈솔도명현증대, 흡기신경원중기방전적빈솔화봉빈솔야현저증대, 이조기화만기방전적빈솔무명현개변; 용상응길항제이후, 상술효응명현피억제。결과제시, 비NMDA수체삼여료쌍상호기신경원지간적교호흥강작용, 병차야개도료흡기신경원적흥강성돌촉수입。
Experiments were performed on in vitro brainstem slice preparations from neonatal rats that retain respiratory network activity. Extracellular recordings were made from 99 neuronal units, respiratory-related or non-respiratory related with rhythmical activity, out of which there were 7 biphasic expiratory and 11 inspiratory ones. Possible roles of non-NMDA receptors in reciprocal excitation among the biphasic expiratory neurons and in excitatory synaptic inputs to inspiratory neurons were investigated by administration of non-NMDA receptor agonist KA and its antagonist DNQX in the perfusion solution. Bath application of non-NMDA receptor agonist KA increased the peak frequency of both biphasic expiratory and inspiratory neuronal discharges, and increased the discharge frequency of the biphasic expiratory neurons and the inspiratory neurons in the middle phase, while the frequency of discharge in the early and late phases were less affected. All of these effects were blocked by addition of the non-NMDA receptor antagonist DNQX, suggesting the involvement of non-NMDA receptors.