Calcium‐dependent potassium conductance in guinea‐pig olfactory cortex neurones in vitro.
Calcium‐dependent potassium conductance in guinea‐pig olfactory cortex neurones in vitro.
复制标题
体外豚鼠嗅皮层神经元的钙依赖性钾电导。
DOI：
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
J. Sim
中科院分区：
文献类型：
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作者：
A. Constanti;J. Sim
1.用单微电极采样-保持技术对豚鼠嗅皮层神经元(23-25℃)进行电压钳制。2.在静息电位(约-80 mV)下，短暂的去极化刺激可诱发出一串动作电位，但几乎看不到后电位。然而，在90%的记录细胞中，膜电位保持在-70 mV和-45 mV之间，去极化电流脉冲引起缓慢的后超极化(a.h.P.)(约8 mV)持续几秒钟，并伴随着输入电导的增加。3.ah.p下的外向膜电流。通过在尖峰列末端快速切换到电压钳位(“混合”钳位)或从-60 mV到-45 mV的电位施加简短的去极化指令来揭示。尾电流呈现明显的上升期(达到峰值的时间约为1 S)和指数衰减期(tau约为3 S)，并被外部钙离子的去除或添加Co2+(1-2 mm)、Cd~(2+)(200微米)或Mg~(2+)(6 Mm)所抑制。美联社。在3 mM-K+介质中，电流翻转电位为-96 mV。4.低浓度(1-2微米)的毒扁豆碱、卡巴胆碱、氧托莫林或毒扁豆碱神经节刺激剂MCN-A-343(1-10微米)均可降低ah.P.电流和漏电导，并诱导出稳定的内向电流，而不影响M-电流(IM)弛豫。肌动抑制一般需要更高的(大于10微米)激动剂浓度，尽管氧托莫林在50微米时仍然无效。5.AHP。电流可被去甲肾上腺素和四乙基铵(TEA)降低，但不能被阿帕明或Tubocurarine所降低。除茶外，这些药剂对IM没有影响。6.加入河豚毒素(TTX，1微米)或去除外源Na+均可抑制ah.p。电压钳位下记录的电流幅度。加入Cd~(2+)或M受体激动剂可进一步降低尾部残存电流。7.正电压指令后诱发的复极化尾电流主要由IM和慢的ah.p组成。电流，几乎没有证据表明钙激活的K+电流(IC)。8.认为慢的ah.p。与IM不同，嗅神经元爆发后后超极化的基础电流是一种钙依赖的K+电流。这表明，胆碱能对这一电流的调制(而不是IM)可能对皮层神经元的细胞兴奋性提供了更微妙的控制。
1. Guinea‐pig olfactory cortex neurones in vitro (23‐25 degrees C) were voltage clamped by means of a single‐micro‐electrode sample‐and‐hold technique. 2. Under current clamp at the resting potential (approximately ‐80 mV), brief depolarizing stimuli evoked trains of action potentials with little visible after‐potential. However, in 90% of recorded cells held at membrane potentials between ‐70 and ‐45 mV, depolarizing current pulses evoked a slow after‐hyperpolarization (a.h.p.) (approximately 8 mV) lasting several seconds and accompanied by an increase in input conductance. 3. The outward membrane current underlying the a.h.p. was revealed either by switching rapidly to voltage clamp at the end of a spike train ('hybrid' clamp) or by applying brief depolarizing commands from potentials between ‐60 to ‐45 mV. The tail current showed a distinct rising phase (time to peak approximately 1 s) and exponential decay (tau approximately 3 s) and was suppressed by removal of external Ca2+, or adding Co2+ (1‐2 mM), Cd2+ (200 microM) or Mg2+ (6 mM). The a.h.p. current reversal potential was ‐96 mV in 3 mM‐K+ medium. 4. Low concentrations (1‐2 microM) of muscarine, carbachol, oxotremorine or the muscarinic ganglion stimulant, McN‐A‐343 (1‐10 microM) reduced the a.h.p. current and leak conductance and induced a steady inward current, without affecting M‐current (IM) relaxations. IM inhibition generally required higher (greater than 10 microM) agonist concentrations, although oxotremorine remained ineffective at up to 50 microM. 5. The a.h.p. current was reduced by noradrenaline and tetraethylammonium (TEA), but not by apamin or tubocurarine. Apart from TEA, these agents had no effect on IM. 6. Addition of tetrodotoxin (TTX, 1 microM) or removing external Na+ depressed the a.h.p. current amplitude recorded under voltage clamp. The residual tail current could be further reduced by adding Cd2+ or muscarinic agonists. 7. Repolarizing tail currents induced following positive voltage commands consisted mainly of IM and slow a.h.p. current with little evidence of a 'fast' Ca2+‐activated K+ current (IC). 8. It is concluded that the slow a.h.p. current that underlies the post‐burst after‐hyperpolarization of olfactory neurones, is a Ca2+‐dependent K+ current distinct from IM. It is suggested that the cholinergic modulation of this current (rather than IM) may provide a more subtle control of cell excitability in cortical neurones.
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影响因子：
5.5
作者：
MADISON, DV;NICOLL, RA
通讯作者：
NICOLL, RA
影响因子：
2.5
作者：
C. Stafstrom;P. Schwindt;M. C. Chubb;W. Crill
通讯作者：
C. Stafstrom;P. Schwindt;M. C. Chubb;W. Crill
影响因子：
56.9
作者：
P. Schwartzkroin;Carl E. Stafstrom
通讯作者：
P. Schwartzkroin;Carl E. Stafstrom
影响因子：
2.5
作者：
JOHNSTON, D;BROWN, TH
通讯作者：
BROWN, TH
哌仑西平区分毒蕈碱受体介导的磷酸肌醇分解和腺苷酸环化酶抑制。
DOI：
--
发表时间：
1985
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Gil,DW;Wolfe,BB
通讯作者：
Wolfe,BB