谷氨酸、γ-氨基丁酸对大鼠前包氏复合体神经元自发放电的影响

EFFECTS OF L-GLUTAMIC ACID AND γ-AMINOBUTYRIC ACID AND THEIR CORRESPONDING ANTAGONISTS ON SPONTANEOUS DISCHARGES OF NEURONS IN PREBOTZINGER COMPLEX IN RATS

用多管微电极技术，在麻醉、自主呼吸的成年大鼠观察了微电泳谷氨酸（L-GLu）、γ-氨基丁酸（GABA）及其拮抗剂DL－2－氨基－5－磷酸戊酸（AP-5）、荷包牡丹碱（BIC）对前包氏复合体（pre－Botzingercomplex，preBotc）区神经元自发放电的影响，并测试了AP-5、BIC分别对L－Glu、GABA效应的阻断作用。结果显示，大多数被测试神经元（37／41个）被L－Glu兴奋，少数（4／41个）无反应：GABA使大多数被测试神经元（34／40个）抑制，对少数神经元（6／40个）无影响。AP-5对神经元放电无影响（19／34个）或产生抑制作用（15／34个）。BIC使神经元兴奋（10／30个）或无反应（20／30个）。L－Glu的兴奋作用和GABA的抑制作用呈量效依赖关系。9／21个受试神经元对L-Glu的兴奋反应被AP-5部分或完全阻断，大多数受试神经元（20／25个）对GABA的抑制反应被BIC部分或完全阻断。上述结果提示，成年大鼠pre－Botc区可能存在着内源性的Glu和GABA，它们分别通过NMDA受体和GABAA受体参与该区的神经信息传递过程。

The effects or iontophoretic application of L-glutamic acid(L-Glu) and -aminobutyric acid (GABA) and their corresponding antagonist DL - 2-amino- 5- phosphonovaleric acid (AP - 5 ) and bicuculline (BIC) on the spontaneous discharges of neurons in the pre-Botzinger complex (pre-Bot c),and the influence of AP-5 and BIC on the effects of L-Glu and GABA respectively,were observed on anesthetized spontaneously breathing Sprague-Dawley adult rats. The results showed that most or the neurons tested(37/41) were excited and a few of them(4/41) were unafrected. Thirty four out of 40 neurons examined were inhibited by GABA and the other 6 were unaffected. AP-5 did not affect (19/34) or Inhibited (15/34) the spontaneous discharges of the neurons tested. BIC showed excitatory effect (10/30) or no effect (20/30) on the spontaneous discharges of the neurons tested. The excitatory effect of L-Gin and the inhibitory effect or GABA showed a dose-response dependent relationship. AP-5 could partially or completely block the excitatory effect of L-Glu on 9 out of 21 neurons tested. BIC could partially or completely block the inhibitory effect of GABA on most of the neurons tested(20/25). These results Indicate that endogenous L-Glu and GABA may exist in the preBot c of the adult rat. They might be Involved in the synaptic transmission of signals in the pre-Bot c by acting on NMDA receptor and GABAA receptor,respectively.