Williams J T, North R A, Tokimasa T
Vollum Institute, Oregon Health Sciences University, Portland 97201.
J Neurosci. 1988 Nov;8(11):4299-306. doi: 10.1523/JNEUROSCI.08-11-04299.1988.
Intracellular recordings were made from rat locus coeruleus neurons in vitro, and membrane currents were measured at potentials from -50 to -130 mV. In the absence of any applied agonists, the slope conductance of the cells increased 3-fold when the cell was hyperpolarized from -60 to -120 mV. This conductance increase was complete within 5 msec of the onset of a hyperpolarizing command and was subsequently independent of time for several seconds. The conductance increase was blocked by cesium chloride (1-2 mM), rubidium chloride (1-2 mM), or barium chloride (1-100 microM). The membrane potential range over which the conductance increased was centered at the potassium equilibrium potential (EK; extracellular potassium concentration, 2.5-10.5 mM): the current/voltage (I/V) relation of the cell could be well described by supposing that there were 2 potassium conductances, one voltage independent (G1) and the other (inward rectifier, Gir) activated according to the expression Gir = Gir,max/(1 + exp[(V - EK)/k]), where k ranged from 15 mV in 2.5 mM potassium to 6 mV in 10.5 mM potassium. The additional membrane potassium conductance that developed when agonists at mu-opioid and alpha 2-adrenoceptors were applied also became larger with membrane hyperpolarization, and this voltage dependence was also reduced or blocked by rubidium, cesium, and barium; in the presence of these agonists the current also reached its final value within 5 msec. However, the conductance increased by the agonists (Gag) was not well expressed by simply increasing the values of G1 and Gir,max. It was best described by a potassium conductance that increased according to Gag,max/(1 + exp[(V - Vm)/k]), where Vm (the potential at which the conductance was half-maximum) was close to the resting potential of the cell.(ABSTRACT TRUNCATED AT 400 WORDS)
在体外对大鼠蓝斑核神经元进行细胞内记录,并在-50至-130 mV的电位下测量膜电流。在未施加任何激动剂的情况下,当细胞从-60 mV超极化至-120 mV时,其斜率电导增加了3倍。这种电导增加在超极化指令开始后的5毫秒内完成,随后在数秒内与时间无关。氯化铯(1-2 mM)、氯化铷(1-2 mM)或氯化钡(1-100 microM)可阻断这种电导增加。电导增加的膜电位范围以钾平衡电位(EK;细胞外钾浓度为2.5-10.5 mM)为中心:假设存在两种钾电导,一种电压非依赖性(G1),另一种(内向整流器,Gir)根据表达式Gir = Gir,max/(1 + exp[(V - EK)/k])激活,其中k在2.5 mM钾时为15 mV,在10.5 mM钾时为6 mV,细胞的电流/电压(I/V)关系可以得到很好的描述。当应用μ-阿片受体和α2-肾上腺素能受体激动剂时,产生的额外膜钾电导也随着膜超极化而增大,这种电压依赖性也可被铷、铯和钡降低或阻断;在这些激动剂存在的情况下,电流也在5毫秒内达到其最终值。然而,激动剂增加的电导(Gag)不能简单地通过增加G1和Gir,max的值来很好地表达。它最好用一种根据Gag,max/(1 + exp[(V - Vm)/k])增加的钾电导来描述,其中Vm(电导为最大值一半时的电位)接近细胞的静息电位。(摘要截断于400字)