Modification of current transmitted from apical dendrite to soma by blockade of voltage- and Ca2+-dependent conductances in rat neocortical pyramidal neurons.
Modification of current transmitted from apical dendrite to soma by blockade of voltage- and Ca2+-dependent conductances in rat neocortical pyramidal neurons.
复制标题
通过阻断大鼠新皮质锥体神经元的电压和 Ca2 依赖性电导来改变从顶端树突传输到体细胞的电流。
DOI：
10.1152/jn.1997.78.1.187
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Crill,WE
中科院分区：
文献类型：
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作者：
Schwindt,PC;Crill,WE
作者：Peter C.和韦恩E. Crill.通过阻断大鼠新皮层锥体神经元中电压和Ca2+依赖性电导对从顶端树突传输到索马的电流的修饰.神经生理学杂志78：187 - 198，1997.用大鼠新皮层锥体神经元的体细胞电压钳技术，测定了谷氨酸在顶树突远端持续离子导入时传递到索马胞体的轴向电流。电压和Ca2+门控通道在顶端树突的证据，寻求通过检查的修改导致膜电位的改变和通道阻断剂的应用程序的这种传输电流。N-甲基-d-天冬氨酸受体阻断后，离子电渗谷氨酸的索马诱发的电流，其幅度与去极化呈线性下降，外推的逆转电位接近0 mV。在相同的条件下，从索马到顶端树突241 - 537 μ m的谷氨酸离子电渗导致了一个传输的轴向电流，该电流在相同的膜电位范围内（约-90到-40 mV）随着去极化而增加。因此，从树突传输到索马的电流在从静息电位（约-70 mV）去极化期间被放大，在超极化期间被衰减。阻断Ca2+内流以消除Ca2+依赖性K+电流后，应用10 mM四乙基氯化铵（TEA）以与树突电压门控K+电流减少一致的方式改变了传输电流的振幅和电压依赖性。我们的结论是，树突状，TEA敏感，电压门控K+通道可以激活紧张性树突状去极化。阻断Ca2+内流的最突出的效果类似于TEA应用引起的效果，这表明这些效果主要是由阻断树突状Ca2+依赖性K+电流引起的。当用乙二醇-双（β-氨基乙基醚）-N，N ′，N ′-四乙酸微电极刺穿细胞以阻止细胞内Ca 2+浓度升高时，阻断Ca 2+内流改变了紧张性传递电流，其方式与阻断高阈值激活的Ca 2+通道携带的内向树突电流的方式一致。我们的结论是，紧张性树突状细胞去极化过程中的Ca 2+流入的主要影响是树突状细胞Ca 2+依赖的K+电流的激活。除了超极化激活的阳离子电流（Ih）外，阻断所有已知的电压门控内向电流不影响传输电流的超极化衰减。细胞外Cs+（3 mM）可逆性地阻断了索马体细胞的超极化衰减。我们的结论是，激活Ih的超极化的近端顶端树突将导致更少的轴向电流到达索马从远端网站比在一个被动的树突。本文还讨论了树突状细胞K~+和Ih通道的几种功能意义。
Schwindt, Peter C. and Wayne E. Crill.Modification of current transmitted from apical dendrite to soma by blockade of voltage- and Ca2+-dependent conductances in rat neocortical pyramidal neurons.J. Neurophysiol.78: 187–198, 1997. The axial current transmitted to the soma during the long-lasting iontophoresis of glutamate at a distal site on the apical dendrite was measured by somatic voltage clamp of rat neocortical pyramidal neurons. Evidence for voltage- and Ca2+-gated channels in the apical dendrite was sought by examining the modification of this transmitted current resulting from the alteration of membrane potential and the application of channel-blocking agents. AfterN-methyl-d-aspartate receptor blockade, iontophoresis of glutamate on the soma evoked a current whose amplitude decreased linearly with depolarization to an extrapolated reversal potential near 0 mV. Under the same conditions, glutamate iontophoresis on the apical dendrite 241–537 μm from the soma resulted in a transmitted axial current that increased with depolarization over the same range of membrane potential (about −90 to −40 mV). Current transmitted from dendrite to soma was thus amplified during depolarization from resting potential (about −70 mV) and attenuated during hyperpolarization. After Ca2+influx was blocked to eliminate Ca2+-dependent K+currents, application of 10 mM tetraethylammonium chloride (TEA) altered the amplitude and voltage dependence of the transmitted current in a manner consistent with the reduction of dendritic voltage-gated K+current. We conclude that dendritic, TEA-sensitive, voltage-gated K+channels can be activated by tonic dendritic depolarization. The most prominent effects of blocking Ca2+influx resembled those elicited by TEA application, suggesting that these effects were caused predominantly by blockade of a dendritic Ca2+-dependent K+current. When cells were impaled with microelectrodes containing ethylene glycol-bis(β-amino-ethyl ether)-N,N′,N′-tetraacetic acid to prevent a rise in intracellular Ca2+concentration, blockade of Ca2+influx altered the tonic transmitted current in different manner consistent with the blockade of a inward dendritic current carried by high-threshold-activated Ca2+channels. We conclude that the primary effect of Ca2+influx during tonic dendritic depolarization is the activation of a dendritic Ca2+-dependent K+current. The hyperpolarizing attenuation of transmitted current was unaffected by blocking all known voltage-gated inward currents except the hyperpolarization-activated cation current (Ih). Extracellular Cs+(3 mM) reversibly abolished both the hyperpolarizing attenuation of transmitted current andIhmeasured at the soma. We conclude that activation ofIhby hyperpolarization of the proximal apical dendrite would cause less axial current to arrive at the soma from a distal site than in a passive dendrite. Several functional implications of dendritic K+andIhchannels are discussed.