Bennett M R, Ho S
Department of Physiology University of Sydney, N.S.W., Australia.
Neurosci Lett. 1992 Mar 16;137(1):41-4. doi: 10.1016/0304-3940(92)90293-g.
Potassium currents in calyciform nerve terminals of the avian ciliary ganglion were analyzed using a single microelectrode voltage clamp. The modulatory affects of adenosine on these currents was also determined. Intracellular CsCl (1 M) blocked the steady-state outward current, indicating that it is mostly carried by K+. Tetraethylammonium (TEA, 10 mM) blocked over 40% of the outward current at a command potential of -30 mV. If Ca2+ influx was blocked by CoCl2 (5 mM), the steady-state outward current was reduced by over 16% in the nerve terminals suggesting that about one fifth of the outward current passes through calcium-activated potassium channels IK(Ca). Adenosine (50 mM) decreased the outward steady-state current over a wide range of command potentials in most terminals studied but failed to decrease this current in the presence of CoCl2 (5 mM). It is concluded that adenosine blocks IK(Ca) in nerve terminals.
使用单微电极电压钳分析了鸡睫状神经节杯状神经末梢中的钾电流。还确定了腺苷对这些电流的调节作用。细胞内氯化铯(1 M)阻断了稳态外向电流,表明其主要由K⁺携带。在 -30 mV 的指令电位下,四乙铵(TEA,10 mM)阻断了超过 40% 的外向电流。如果用氯化钴(5 mM)阻断 Ca²⁺ 内流,神经末梢中的稳态外向电流减少超过 16%,这表明约五分之一的外向电流通过钙激活钾通道 IK(Ca)。在大多数研究的神经末梢中,腺苷(50 mM)在很宽的指令电位范围内降低了外向稳态电流,但在存在氯化钴(5 mM)的情况下未能降低该电流。结论是腺苷阻断神经末梢中的 IK(Ca)。