Contribution of the low-threshold T-type calcium current in generating the post-spike depolarizing afterpotential in dentate granule neurons of immature rats.
作者信息
Zhang L, Valiante T A, Carlen P L
机构信息
Playfair Neuroscience Unit, Toronto Hospital Research Institute, University of Toronto, Ontario, Canada.
The underlying ionic mechanisms of the postspike depolarizing afterpotential (DAP) in hippocampal dentate granule (DG) neurons of immature rats (postnatal 7- to 17-day-old) were examined using whole cell patch recordings in brain slices. 2. In current-clamp mode, the DAP followed each single action potential. Graded DAP-like responses were also evoked by depolarizing current pulses when the action potential was blocked by tetrodotoxin (TTX), demonstrating that the TTX-sensitive Na+ conductance is not necessary for DAP generation. The membrane resistance near the DAP peak was lower than at rest, suggesting activation of inward currents rather than blockade of outward currents during the DAP. The DAP peak amplitude showed a strong dependence on voltage, increasing with membrane hyperpolarization and decreasing with depolarization in the range of -90 to -50 mV. Repetitive stimulation at 1-2 Hz did not change the amplitude or decay of the DAP or DAP-like response. 3. Bath application of 2 mM 4-aminopyridine (4-AP) and 5 mM tetraethylammonium chloride (TEA) prolonged the action potential and enhanced the DAP, suggesting that the DAP waveform is determined by the interaction of voltage-activated outward K+ currents and inward currents. 4. Bath application of 2 mM Co2+ depressed the DAP and the DAP-like potential. Replacement of extracellular Ca2+ with Ba2+ potentiated the DAP. Intracellular Ca2+ chelation with the fast chelator, bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA), only slightly enhanced the DAP, suggesting that the DAP is not generated by inward currents activated secondary to Ca2+ influx.(ABSTRACT TRUNCATED AT 250 WORDS)
摘要
采用脑片全细胞膜片钳记录技术，研究了未成熟大鼠（出生后7至17天）海马齿状颗粒（DG）神经元锋电位后去极化后电位（DAP）的潜在离子机制。2. 在电流钳模式下，DAP跟随每个单动作电位。当动作电位被河豚毒素（TTX）阻断时，去极化电流脉冲也可诱发分级的DAP样反应，表明DAP的产生不需要TTX敏感的Na⁺电导。DAP峰值附近的膜电阻低于静息时，提示DAP期间内向电流激活而非外向电流阻断。DAP峰值幅度强烈依赖电压，在-90至-50 mV范围内随膜超极化增加而增加，随去极化而降低。1至2 Hz的重复刺激不会改变DAP或DAP样反应的幅度或衰减。3. 浴用2 mM 4-氨基吡啶（4-AP）和5 mM四乙铵氯化物（TEA）可延长动作电位并增强DAP，提示DAP波形由电压激活的外向K⁺电流和内向电流的相互作用决定。4. 浴用2 mM Co²⁺可抑制DAP和DAP样电位。用Ba²⁺替代细胞外Ca²⁺可增强DAP。用快速螯合剂双（邻氨基苯氧基）-N,N,N',N'-四乙酸（BAPTA）进行细胞内Ca²⁺螯合仅轻微增强DAP，提示DAP不是由Ca²⁺内流继发激活的内向电流产生的。（摘要截断于250字）
