Fass D M, Levitan E S
Department of Neuroscience, University of Pittsburgh, Pennsylvania 15261, USA.
J Gen Physiol. 1996 Jul;108(1):1-11. doi: 10.1085/jgp.108.1.1.
Whole-cell L-type Ca2+ channel current was recorded in GH3 clonal rat pituitary cells using Ba2+ as a charge carrier. In the presence of the dihydropyridine agonist Bay K 8644, deactivation was best described by two exponential components with time constants of approximately 2 and approximately 8 ms when recorded at -40 mV. The slow component activated at more negative potentials than the fast component: Half-maximal activation for the slow and fast components occurred at approximately -15 and approximately 1 mV, respectively. The fast component was more sensitive to enhancement by racemic Bay K 8644 than the slow component: ED50fast = approximately 21 nM, ED50slow = approximately 74 nM. Thyrotropin-releasing hormone (TRH; 1 microM) inhibited the slow component by approximately 46%, whereas the fast component was inhibited by approximately 22%. TRH inhibition of total L-current showed some voltage dependence, but each Bay K 8644-revealed component of L-current was inhibited in a voltage-independent manner. Therefore, the apparent voltage dependence of TRH action is derived from complexities in channel gating rather than from relief of inhibition at high voltages. In summary, Bay K 8644-enhanced L-currents in GH3 cells consist of two components with different sensitivities to voltage, racemic Bay K 8644, and the neuropeptide TRH.
采用Ba2+作为电荷载体,在GH3克隆大鼠垂体细胞中记录全细胞L型Ca2+通道电流。在二氢吡啶激动剂Bay K 8644存在的情况下,当在-40 mV记录时,失活最好用两个指数成分来描述,时间常数分别约为2 ms和约8 ms。慢成分比快成分在更负的电位下激活:慢成分和快成分的半数最大激活分别发生在约-15 mV和约1 mV。快成分比慢成分对消旋Bay K 8644的增强更敏感:ED50快约为21 nM,ED50慢约为74 nM。促甲状腺激素释放激素(TRH;1 μM)抑制慢成分约46%,而快成分被抑制约22%。TRH对总L电流的抑制表现出一定的电压依赖性,但L电流的每个Bay K 8644揭示成分均以电压非依赖性方式被抑制。因此,TRH作用的表观电压依赖性源于通道门控的复杂性,而非高电压下抑制的解除。总之,Bay K 8644增强的GH3细胞L电流由两个对电压、消旋Bay K8644和神经肽TRH具有不同敏感性的成分组成。