Presynaptic calcium-activated potassium channels and calcium channels at a crayfish neuromuscular junction.
Presynaptic calcium-activated potassium channels and calcium channels at a crayfish neuromuscular junction.
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突触前钙激活钾通道和小龙虾神经肌肉接头处的钙通道。
DOI：
10.1152/jn.1995.73.1.178
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Bittner,GD
中科院分区：
文献类型：
--
作者：
Blundon,JA;Wright,SN;Brodwick,MS;Bittner,GD
1.本研究采用双微电极电流钳技术，研究了淡水螯虾步行腿兴奋性神经肌肉接头突触前末梢Ca（2+）激活的K+电导[gK（Ca）]和Ca（2+）电导（gCa）以及递质释放的各种特性。2.电压激活的Na+电导（gNa）和K+电导[gK（v）]分别用河豚毒素和3，4-二氨基吡啶阻断。在这些条件下，由第一（调节）脉冲产生的突触前去极化允许Ca 2+进入突触前末梢并激活gK（Ca），其调制由第二（测试）脉冲产生的去极化的幅度。在测试脉冲下测量的gK（Ca）的相对量随着调节脉冲的幅度或持续时间的增加而增加。3.一个短暂的超极化后立即调节脉冲大大降低gK（Ca）。4. gK（Ca）激活被漏斗网蜘蛛毒素（一种Ca ~（2+）通道阻断剂）阻断或通过注射具有钙螯合剂双-（邻氨基苯氧基）-N，N，N '，N'-四乙酸（BAPTA）的突触前末端区域来阻断。在电流钳条件下，gK（Ca）不被Charybdotoxin或iberiotoxin [特异性gK（Ca）阻断剂]阻断。5.当gK（Ca）被阻断或降低时，动作电位的去极化后电位幅度增加。当gK（v）被阻断或降低时，动作电位时程增加。6.细胞内注射BAPTA到突触前末端区域消除诱发神经递质释放之前，测试脉冲调制的影响，这表明，K（Ca）通道有一个更大的敏感性（更大的亲和力或更低的化学计量比）Ca 2+比发射机释放机械。BAPTA减少神经递质释放66- 78%，但不影响促进神经递质释放。7.当gNa，gK（v），和gK（Ca）被阻断时，我们检测到由突触前gCa增加产生的膜去极化，其被2 mM Cd 2+或0 mM Ca 2+消除。
1. We used a two-microelectrode current clamp to investigate various characteristics of the Ca(2+)-activated K+ conductance [gK(Ca)] and Ca2+ conductance (gCa), and transmitter release in presynaptic terminals of excitatory neuromuscular junctions in the crayfish walking leg. 2. Voltage-activated Na+ conductances (gNa) and K+ conductances [gK(v)] were blocked with tetrodotoxin and 3,4-diaminopyridine, respectively. Under these conditions, presynaptic depolarization produced by a first (conditioning) pulse admitted Ca2+ into the presynaptic terminals and activated gK(Ca), which modulated the amplitude of the depolarization produced by a second (test) pulse. The relative amount of gK(Ca) measured at the test pulse increased with increased magnitude or duration of the conditioning pulse. 3. A brief hyperpolarization immediately after a conditioning pulse substantially reduced gK(Ca). 4. gK(Ca) activation was blocked by funnel web spider toxin (a Ca2+ channel blocker) or by injection of the presynaptic terminal region with a calcium chelator, bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA). Under current-clamp conditions, gK(Ca) was not blocked by charybdotoxin or iberiotoxin [specific gK(Ca) blockers]. 5. When gK(Ca) was blocked or reduced, the amplitude of the depolarizing afterpotential of action potentials was increased. When gK(v) was blocked or reduced, the duration of action potentials was increased. 6. Intracellular injection of BAPTA into the presynaptic terminal region eliminated evoked neurotransmitter release before test pulse modulation was affected, suggesting that the K(Ca) channel had a greater sensitivity (greater affinity or lower stoichiometry) for Ca2+ than did the transmitter release machinery. BAPTA reduced neurotransmitter release by 66-78%, but did not affect facilitation of neurotransmitter release. 7. When gNa, gK(v), and gK(Ca) were blocked, we detected a membrane depolarization produced by an increase in presynaptic gCa that was eliminated by 2 mM Cd2+ or 0 mM Ca2+.