Somatostatin activates an inwardly rectifying K+ conductance in freshly dispersed rat somatotrophs.
Somatostatin activates an inwardly rectifying K+ conductance in freshly dispersed rat somatotrophs.
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生长抑素可激活新鲜分散的大鼠生长激素细胞中的内向整流 K 电导。
DOI：
10.1113/jphysiol.1991.sp018770
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
J. Kraicer
中科院分区：
文献类型：
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作者：
S. M. Sims;B. Lussier;J. Kraicer
1. 在传统的全细胞和穿孔贴片配置中，使用膜片钳记录方法在分离后 16 小时内对来自酶促分散的大鼠垂体前叶的生长激素进行了研究，通过密度梯度离心富集至纯度超过 94%。 2. 在使用穿孔贴片技术研究的 52 个细胞中，有 36 个细胞的膜电位节律振荡产生了动作电位。膜电位在约 ‐70 mV 和约 ‐25 mV 之间振荡，平均频率（平均值 +/- S.D.）为 0.9 +/- 0.9 s-1。 3. 电池的电流-电压 (I-V) 关系在负电位下呈线性，在正电位至 ‐40 mV 时向外整流。外向电流是由 K+ 通道引起的证据来自失活尾电流，其反转方向接近 K+ 平衡电位 (EK)。外部 K+ 浓度 ([K+]o) 每变化十倍，反转电位就会移动 60 mV，正如 K+ 电流所预期的那样。 4.四乙铵（TEA）对外向电流的抑制为K+电流提供了额外的证据。 Cd2+ 减少了外向电流，表明存在 Ca(2+) 激活的 K+ 电导。 5. 去极化命令引发瞬态内向 Na+ 电流和持续 Ca2+ 电流 (ICa)。 ICa 在记录移液器中与 Cs+ 和 TEA 隔离记录，并以 10 mM-Ba2+ 作为电荷载体。 ICa 的激活在大约 ‐40 mV 时开始，峰值内向电流为 0 至 +10 mV。半失活电位约为‐35 mV。此外，硝苯地平可阻断ICa。这些特征表明生长激素细胞中存在 L 型 Ca2+ 通道。 6.生长抑素引起超极化并抑制动作电位的自发爆发。在电压钳位下，生长抑素激活内向整流电流，该电流在 EK 附近反转方向。当 [K+]o 的升高改变 EK 时，[K+]o 每变化 10 倍，生长抑素诱导的电流的反转电位就会改变 55 mV，正如根据能斯特关系对 K+ 电流所预测的那样。生长抑素诱导的电导 (gK) 在更负的电位下更大，并且激活范围随着 [K+]o 的升高而正向移动。 7. 我们得出结论，新鲜分离的大鼠生长激素细胞具有 Na+、Ca2+ 和 K+ 电流。大部分细胞表现出自发的动作电位爆发。生长抑素激活内向整流 K+ 电导，导致自发动作电位活动超极化和停止，这些活动有助于抑制生长激素释放。
1. Somatotrophs from enzymatically dispersed anterior pituitary glands of rats, enriched to greater than 94% purity by density gradient centrifugation, were studied within 16 h of isolation using patch clamp recording methods in the conventional whole‐cell and the perforated‐patch configurations. 2. Rhythmic oscillations of membrane potential gave rise to action potentials in thirty‐six of fifty‐two cells studied with the perforated‐patch technique. Membrane potential oscillated between approximately ‐70 mV and approximately ‐25 mV with an average frequency (mean +/‐ S.D.) of 0.9 +/‐ 0.9 s‐1. 3. The current‐voltage (I‐V) relationship of cells was linear at negative potentials with outward rectification at potentials positive to ‐40 mV. Evidence that the outward current was due to K+ channels came from the deactivation tail currents, which reversed direction close to the K+ equilibrium potential (EK). The reversal potential shifted 60 mV per tenfold change of external K+ concentration ([K+]o), as expected for K+ current. 4. Suppression of outward current by tetraethylammonium (TEA) provided additional evidence for K+ current. Cd2+ reduced outward current, suggesting the presence of Ca(2+)‐activated K+ conductance. 5. Depolarizing commands elicited transient inward Na+ current and a sustained Ca2+ current (ICa). ICa was recorded in isolation with Cs+ and TEA in the recording pipette and 10 mM‐Ba2+ as the charge carrier. Activation of ICa began at approximately ‐40 mV, with peak inward current at 0 to +10 mV. The half‐inactivation potential was approximately ‐35 mV. In addition, ICa was blocked by nifedipine. These characteristics indicate the presence of L‐type Ca2+ channels in somatotrophs. 6. Somatostatin caused hyperpolarization and suppressed the spontaneous bursts of action potentials. Under voltage clamp, somatostatin activated an inwardly rectifying current that reversed direction near EK. When EK was altered by elevation of [K+]o, the reversal potential of the somatostatin‐induced current shifted 55 mV per tenfold change of [K+]o, as predicted for a K+ current by the Nernst relation. The somatostatin‐induced conductance (gK) was greater at more negative potentials, and the activation range shifted positive with elevation of [K+]o. 7. We conclude that freshly isolated rat somatotrophs possess Na+, Ca2+ and K+ currents. A large proportion of the cells exhibit spontaneous bursts of action potentials. Somatostatin activates an inwardly rectifying K+ conductance, causing hyperpolarization and cessation of spontaneous action potential activity, actions that would contribute to suppression of growth hormone release.