Somatic amplification of distally generated subthreshold EPSPs in rat hippocampal pyramidal neurones
Somatic amplification of distally generated subthreshold EPSPs in rat hippocampal pyramidal neurones
复制标题
DOI：
10.1111/j.1469-7793.1999.0085o.x
复制
发表时间：
1999-08-15
影响因子：
5.5
通讯作者：
Lambert, JDC
中科院分区：
文献类型：
--
作者：
Andreasen, M;Lambert, JDC
1. 海马CA1锥体神经元的细胞内记录显示，选择性刺激远端三分之一的顶端树突的传入输入所诱发的epsp对树突膜电位（V-m）的变化相对不敏感，但被体细胞V-m的去极化放大。这种扩增出现在静息膜电位（RMP）的去极化电位，但在epsp接近动作电位产生的阈值时最为明显。放大由均匀分量和可变分量组成，只有当epsp跨越阈值时才存在。体细胞扩增是由内源性膜电流引起的，而内源性膜电流被体细胞施加的河蟹毒素（TTX, 10 μ M）阻断，但对NiCl2 （100-200 μ M）不敏感。因此，我们认为阈下EPSP的扩增主要是由于非失活Na+电流（I-NaP）的激活。在树突内记录期间注射4-氨基吡啶（4-AP, 25-50 mM），导致37%的树突中epsp扩增，这与在体细胞记录中观察到的结果相似。然而，在TTX在体细胞应用的一个案例中，树突扩增被阻断，这表明它是体细胞扩增的反映。由于向可变放大的转变是非常突然的，并且只存在于接近阈值的非常窄的电压范围内，我们认为可变成分是由I-NaP的再生激活引起的。变化本身可能是由于同时激活不同的向外K+电流。目前的研究结果表明，CA1锥体神经元的体细胞区域可以作为远端诱发epsp的电压依赖性放大器，这是由于体细胞I-NaP的激活。这种放大机制的存在将对远端产生的epsp的整合方式产生重要的功能后果。
1. Intracellular recordings from hippocampal CA1 pyramidal neurones revealed that EPSPs evoked by selective stimulation of the isolated afferent input to the distal third of the apical dendrites were relatively insensitive to changes in dendritic membrane potential (V-m) but amplified by depolarizations of the somatic V-m. The amplification was present at potentials depolarized from resting membrane potential (RMP) but was most marked when the EPSPs were close to threshold for action potential generation. The amplification consisted of a uniform component and a variable component which was only present when the EPSPs were threshold straddling.2. The somatic amplification was caused br an intrinsic membrane current which was blocked by somatic application of tetrodotoxin (TTX, 10 mu M), but, was insensitive to bath application of NiCl2, (100-200 mu M). We therefore suggest that the amplification of the subthreshold EPSP is due primarily to the activation of a non-inactivating Na+ current (I-NaP).3. Injection of 4-aminopyridine (4-AP, 25-50 mM) during intradendritic recordings resulted in amplification of the EPSPs in 37 % of the dendrites, which was similar to that observed in somatic recordings. However, in the one case in which somatic application of TTX was tested, dendritic amplification was blocked, suggesting that it is a reflection of the somatic amplification.4. Because the shift to variable amplification was very abrupt and it is present in only a very narrow voltage range close to threshold, we suggest that the variable component is caused by the regenerative activation of I-NaP. The variability itself is probably due to the simultaneous activation of different outward K+ currents.5. The present results indicate that the somatic region of CA1 pyramidal neurones can function as a voltage-dependent amplifier of distally evoked EPSPs and that this is due to the activation of a somatic I-NaP. The presence of this amplifying mechanism will have important functional consequences for the way in which distally generated EPSPs are integrated.