Inhibition of Ca2+ conductance in identified leech neurons by benzodiazepines.
Inhibition of Ca2+ conductance in identified leech neurons by benzodiazepines.
复制标题
苯二氮卓类药物对已鉴定的水蛭神经元中 Ca2+ 电导的抑制作用。
DOI：
10.1073/pnas.82.11.3935
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发表时间：
1985
影响因子：
11.1
通讯作者：
DeLorenzo,RJ
中科院分区：
文献类型：
--
作者：
Johansen,J;Taft,WC;Yang,J;Kleinhaus,AL;DeLorenzo,RJ
Benzodiazepines (BZs) in micromolar concentrations inhibit Mn2+- and Co2+-sensitive regenerative divalent cation potentials, which are revealed in the presence of tetraethylammonium ion, in leech nociceptive neurons (N cells). This BZ effect is reversible and dose-dependent. The BZs, like Mn2+ and Co2+, inhibit the maximum rate of depolarization (Vmax) and duration of divalent cation potentials at concentrations that do not significantly affect resting membrane potential or Vmax of the Na+-dependent action potential. Ultraviolet-induced BZ binding to micromolar-affinity sites in ganglia and isolated cells irreversibly blocks Ca2+ conductance in neurons without significantly affecting resting membrane potentials. BZ binding studies with leech neuronal membrane show saturable, specific binding in the micromolar concentration range that was similar to BZ binding to synaptosomal membrane fractions. The apparent Kd obtained from the micromolar-affinity BZ binding curve for leech ganglionic membrane preparations agrees well with the apparent Ki estimated from the dose-response curve measuring BZ inhibition of Vmax of the divalent cation potentials. These findings indicate that BZs act like Ca2+-channel antagonists in intact neuronal preparations and are consistent with the hypothesis that BZ binding to micromolar-affinity receptors modulates voltage-gated Ca2+ channels.
