CONCENTRATION OF CARBON-DIOXIDE, INTERSTITIAL PH AND SYNAPTIC TRANSMISSION IN HIPPOCAMPAL-FORMATION OF THE RAT
CONCENTRATION OF CARBON-DIOXIDE, INTERSTITIAL PH AND SYNAPTIC TRANSMISSION IN HIPPOCAMPAL-FORMATION OF THE RAT
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DOI：
10.1113/jphysiol.1988.sp016961
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发表时间：
1988-02-01
影响因子：
5.5
通讯作者：
SOMJEN, GG
中科院分区：
文献类型：
--
作者：
BALESTRINO, M;SOMJEN, GG
用离子选择微电极测量氨基甲酸乙酯麻醉大鼠齿状筋膜间质pH (pHo)，通过改变肺通风量和吸入空气CO2含量来控制CO2水平。在海马组织切片的CA1区，通过改变气相中的CO2，或通过向浴液的人工脑脊液（ACSF）中添加HCl或NaOH，或通过改变HCO3-的浓度，体外测量和改变pHo。正侧诱发复合动作电位（“群体尖峰”）在高碳酸血症时降低，在低碳酸血症时升高。在完整脑齿状筋膜中，ph值每变化0.1，颗粒细胞的群体峰值平均变化幅度超过对照幅度的40%。在CA1区组织切片中，CO2或HCO3-引起的pH值每改变0.1，群体尖峰幅度的变化约为30%，而HCl或NaOH引起的pH值每改变0.1，群体尖峰幅度的变化约为15%。麻醉大鼠在一定刺激强度下引起的局灶突触电位（FEPSP）受[CO2]变化的影响较弱；在组织切片中，对FEPSP的弱作用不一致。在原位和离体海马中，由一定强度的FEPSP触发的种群峰值在低碳酸血症中增加，在高碳酸血症中减少。这表明CO2主要影响突触后细胞的电兴奋性，对递质释放和递质与受体的相互作用影响很小或没有影响。麻醉大鼠高碳酸血症通常伴有齿状筋膜[K+]o的轻微升高。组织[Ca2+]o变化不大且不一致。这两种离子，以及伴随的血压或组织氧分压（Pt, O2）的变化，都不能解释pH值对神经元兴奋性的影响。结果表明，增加H+离子细胞外浓度对海马神经元放电阈值有中等抑制作用。升高的[CO2]和降低的[HCO3-]的更强的作用可能是对神经元膜的直接影响。大脑通过调节呼吸来控制自身的兴奋性。
Interstitial pH (pHo) was mesured with ion-selective microelectrodes in the fascia dentata of rats anaesthetized with urethane, while CO2 levels were controlled by varying pulmonary ventilation and CO2 content of inspired air. In the CA1 sector of hippocampal tissue slices in vitro pHo was similarly measured and altered by varying CO2 in the gas phase, or by adding HCl or NaOH to the artificial cerebrospinal fluid (ACSF) of the bath, or by changing the concentration of HCO3-. Orthodromically evoked compound action potentials (''population spikes'') were depressed in hypercapnia and increased in hypocapnia. In the fascia dentata of intact brains the population spike of the granule cells varied on average by more than 40% of control amplitude for each 0.1 change of pHo. In the CA1 zone of tissue slices in vitro, the change of population spike amplitude was approximately 30% per pH change of 0.1 caused by altered CO2 or HCO3- concentration, but only about 15% per pH change of 0.1 when HCl or NaOH wer administered. In anesthetized rats the focal synaptic potential (FEPSP) evoked by a given stimulus intensity was weakly influenced by varying [CO2]; in tissue slices weak effects on FEPSP were inconsistent. In hippocampus both in situ and in vitro the population spike triggered by a given magnitude of FEPSP increased in hypocapnia and decreased in hypercapnia. This suggests that the main effect of CO2 is on the electric excitability of postsynaptic cells, minor or no effect on transmitter release and on the interaction of the transmitter with its receptors. Hypercapnia of anaesthetized rats was usually associated with a slight increase of [K+]o in the fascia dentata. Tissue [Ca2+]o changed little and not consistently. Neither of these two ions, nor concomitant changes of blood pressure or tissue partial pressure of oxygen, (Pt, O2), could account for the effects of pH on neuronal excitability. The results show that increasing the extracellular concentration of H+ ions has a moderately depressant effect on the firing threshold of hippocampal neurones. The more powerful effects of elevated [CO2] and of lowered [HCO3-] may probably be explained by a direct effect on the neuronal membrane. The brain, by regulating breathing, controls its own excitability.