Muscarinic modulation of conductances underlying the afterhyperpolarization in neurons of the rat basolateral amygdala.
Muscarinic modulation of conductances underlying the afterhyperpolarization in neurons of the rat basolateral amygdala.
复制标题
大鼠基底外侧杏仁核神经元后超极化的毒蕈碱调节电导。
DOI：
10.1016/0006-8993(93)90301-3
复制
发表时间：
1993
期刊：
影响因子：
2.9
通讯作者：
Moises,HC
中科院分区：
文献类型：
--
作者：
Womble,MD;Moises,HC
激活M受体后，杏仁基底外侧核(BLA)锥体神经元的兴奋性水平显著增加，这一效应与动作电位放电速度的增加和后超极化(AHP)的减少有关。我们用单个微电极穿透大鼠前脑腹侧脑片的BLA锥体神经元，以检测AHP和棘波频率调节的电流，并确定它们对毒碱调制的敏感性。在电压钳中，去极化步骤之后是两相外向尾流，由快速衰减(IFast)和缓慢衰减(Islow)电流分量组成。它们分别与AHP的中等和慢速部分在时间上相对应。随着胞外K+浓度的增加，AHP尾电流的反转电位或第一分量向去极化方向移动。在0-Ca~(2+)介质灌流或TEA(1-5 mm)或氨基甲胆碱(10-40μM)灌流时，IFast值降低。提示IFasti是由迅速衰减的钙激活钾电流(IC)和毒鼠碱敏感的M电流(IM)产生的。在含有正常或升高K+的介质中，低尾电流分量与EK的估计值相反。在记录电极中灌流0-Ca~(2+)介质或加入环-AMP可消除该组分。TEA(5 MM)或阿帕明(5 0~5 0 0 nM)对其无阻断作用，但可被卡巴胆碱剂量依赖性地抑制(IC50=0.5μM)。电刺激BLA的胆碱能传入通路对ISlow产生抑制作用，这种作用可被eserine增强，而被阿托品阻断。ISlow成分的丧失总是伴随着类似的住宿减少和缓慢的AHP。推测该尾流成分是由缓慢衰减的钙激活钾电流IAHP引起的。因此，对IAHP的毒碱抑制有助于胆碱能刺激后BLA锥体神经元表现出的兴奋性增强。
The excitability level of pyramidal neurons in the basolateral amygdala (BLA) is greatly increased following muscarinic receptor activation, an effect associated with an increased rate of action potential firing and reduction of the afterhyperpolarization (AHP). We impaled BLA pyramidal neurons in slices of rat ventral forebrain with a single microelectrode to examine the currents underlying the AHP and spike frequency accomodation and determine their sensitivities to muscarinic modulation. In voltage-clamp, depolarizing steps were followed by biphasic outward tail currents, consisting of rapidly decaying (IFast) and slowly decaying (ISlow) current components. These corresponded temporally with the medium and slow portions of the AHP, respectively. The reversal potential or theIFastcomponent of the AHP tail current shifted in the depolarizing direction with increases in the extracellular K+concentration. The amplitude ofIFastwas reduced during perfusion of 0-Ca2+medium or by superfusion of TEA (1–5 mM) or carbachol (10–40 μM). It is suggested thatIFastwas produced by the rapidly decaying Ca2+-activated K+current (IC) and the muscarinic-sensitive M-current (IM). TheISlowtail current component reversed at the estimated values forEKin medium containing either normal or elevated K+levels. This component was eliminated by perfusion of 0-Ca2+medium or inclusion of cyclic-AMP in the recording electrode. It was not blocked by TEA (5 mM) or apamin (50–500 nM), but was reduced by carbachol in a dose-dependent manner (IC50=0.5 μM). Electrical stimulation cholinergic afferent pathways to the BLA produced inhibition ofISlow, an effect which was enhanced by eserine and prevented by atropine. Loss of theISlowcomponent was always accompanied by similar reductions in accomodation and the slow AHP. It was concluded that this tail current component resulted from the slowly decaying Ca2+-activated K+current,IAHP. Thus, the muscarinic inhibition ofIAHPcontributes to the enhanced excitability exhibited by BLA pyramidal neurons following cholinergic stimulation.