RATE CONSTANTS ASSOCIATED WITH CHANGES IN SODIUM CONDUCTANCE IN AXONS PERFUSED WITH SODIUM FLUORIDE
RATE CONSTANTS ASSOCIATED WITH CHANGES IN SODIUM CONDUCTANCE IN AXONS PERFUSED WITH SODIUM FLUORIDE
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DOI：
10.1113/jphysiol.1970.sp009299
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发表时间：
1970-01-01
影响因子：
5.5
通讯作者：
MEVES, H
中科院分区：
文献类型：
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作者：
CHANDLER, WK;MEVES, H
1. 轴突经300 mM - NaF灌注，置于- 0·3-4°c无K人工海水中，测量了阶跃去极化过程中的膜电流。Na电导采用改进的Hodgkin-Huxley模型，gNa=ḡNam3（h1+h2）。假设h1和h2的变化遵循[公式：见文本]，其中表示非活动状态。所得到的速率常数和稳态值与霍奇金-赫胥黎方程一致，只是m∞3对v的实验关系向负方向偏移了10-15 mV。这种差异，在胆碱海水实验中没有发现，可以根据电压测量电极之间膜的串联电阻来解释。在0℃条件下，(αh2+ βh2) =p(D2+ 2) = 0.55 msec−1，用βh1= 0.5 /{exp[−(V+ 32)/10] +D1exp(−V/V1)}, αh2=pexp (V/V2), βh2=pexp (V/V2−V/23·5)+pD2拟合h和h2变化的速率常数（msec−1）。实验给出的平均值为d1 = 3.6,V1= 240 mV,p= 0.08 msec - 1, v2 = 70 mV。平均值ofḡNawas 66 mmho/cm2.4。当负电压∞3对vis较陡时，Na海水中轴突的βh1和αh2/βh2的点不能很好地拟合，而胆碱海水中轴突的数据可以很好地拟合。这些差异可以根据一个串联电阻来解释。在16-17°C测得thatḡNahas aq10为1.6，τm - 1aq10为2.8，β h1aq10为3.5。αh2/βh2的比值相对于0℃时降低，可用q10 = 0·6.6拟合。用250 mM‐NaF + 50 mM‐KF进行的测量得到的速率常数与用300 mM‐NaF得到的速率常数非常相似。与300 mM‐NaF相比，300 mM‐KF灌注的βh1值增加了一倍，αh2/βh2降低了约一半。α - h2的电压依赖性使得失活态的去极化恢复可能发生在viax→h1而不是x→h2→h1。
1. Membrane currents during step depolarizations were measured in axons which were perfused with 300 mM‐NaF and placed in K‐free artificial sea‐water, −0·3–4° C. The Na conductance was fitted by the modified Hodgkin—Huxley model,gNa=ḡNam3(h1+h2). Changes inh1andh2were assumed to follow [Formula: see text] wherexrepresents the inactive state.2. The rate constants and steady‐state values formwere in agreement with the Hodgkin—Huxley equations except that the experimental relationship ofm∞3againstVwas shifted 10–15 mV in the negative direction. This discrepancy, which was not found in an experiment with choline sea‐water, can be explained on the basis of a resistance in series with the membrane between the voltage measuring electrodes.3. At 0° C the rate constants (in msec−1) associated with changes inh1andh2were fitted using the following equations: βh1= 0·5/{exp [− (V+ 32)/10] +D1exp (−V/V1)}, αh2=pexp (V/V2), βh2=pexp (V/V2−V/23·5) +pD2, with the condition that at 0 mV, (αh2+ βh2) =p(D2+ 2) = 0·55 msec−1. The experiments gave average valuesD1= 3·6,V1= 240 mV,p= 0·08 msec−1andV2= 70 mV. The average value ofḡNawas 66 mmho/cm2.4. At negative voltages wherem∞3againstVis steep, the points for βh1and αh2/βh2from axons in Na sea‐water were not fitted well by the above equations whereas data from an axon in choline sea‐water were. These discrepancies can be explained on the basis of a series resistance.5. Measurements made at 16–17° C indicated thatḡNahas aQ10of 1·6, τm−1aQ10of 2·8 and βh1aQ10of 3·5. The ratio αh2/βh2was decreased relative to the value at 0° C and could be fitted by usingQ10= 0·6.6. Measurements made with 250 mM‐NaF + 50 mM‐KF inside gave rate constants which were very similar to those obtained with 300 mM‐NaF. Perfusion with 300 mM‐KF appeared to double the value of βh1, relative to that obtained with 300 mM‐NaF, and to reduce αh2/βh2by about half.7. The voltage dependence of αh2makes it likely that following depolarization recovery from the inactive statexoccurs viax→h1rather thanx→h2→h1.