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豚鼠海马切片中突触传递长时程增强的可能机制。

Possible mechanisms for long-lasting potentiation of synaptic transmission in hippocampal slices from guinea-pigs.

作者信息

Andersen P, Sundberg S H, Sveen O, Swann J W, Wigström H

出版信息

J Physiol. 1980 May;302:463-82. doi: 10.1113/jphysiol.1980.sp013256.

Abstract
  1. Long-lasting potentiation of synaptic transmission was studied in the CA1 region of guinea-pig hippocampal slices maintained in vitro. 2. Stimulating pulses were delivered alternately to two independent afferent pathways, stratum radiatum and stratum oriens. The presynaptic volleys and field e.p.s.p.s. were recorded from the same two layers, while an electrode in the pyramidal cell body layer recorded the population spike or in other experiments the extra- or intracellular potentials from a single pyramidal cell. 3. A short tetanus to either of the two input pathways produced a long-lasting enhancement of the field e.p.s.p. as well as an increased size and a reduced latency of the population spike. This long-lasting potentiation was observed for up to 110 min after tetanization. Extracellular unit recordings showed that this potentiation is accompanied by an increased probability of firing and a reduced firing latency. Intracellular recordings showed an increased e.p.s.p., through the increase was smaller and less regular than for the extracellular field e.p.s.p. 4. No corresponding changes were seen in the field potential responses to stimulation of the untetanized input path, or in the intracellularly measured soma membrane potential, resistance, or excitability. The latter two properties were measured by intracellular injection of current pulses. It is concluded that long-lasting potentiation is specific to the pathway which has received the tetanization. 5. Following tetanization there was also a short-lasting (usually 2-4 min) depression, most often seen for the control pathway but sometimes visible on the tetanized side as well, superimposed on the potentiation. It is concluded that the short-lasting depression is not confined to any particular pathway but is a generalized (unspecific) phenomenon.
摘要
  1. 在体外培养的豚鼠海马切片的CA1区研究了突触传递的长时程增强。2. 刺激脉冲交替施加于两条独立的传入通路,即辐射层和原层。在相同的两层记录突触前群峰电位和场兴奋性突触后电位,而在锥体细胞层的一个电极记录群体峰电位,或者在其他实验中记录单个锥体细胞的细胞外或细胞内电位。3. 对两条输入通路中的任何一条进行短串刺激,都会使场兴奋性突触后电位产生长时程增强,同时群体峰电位的幅度增大、潜伏期缩短。在强直刺激后长达110分钟内都能观察到这种长时程增强。细胞外单位记录显示,这种增强伴随着放电概率的增加和放电潜伏期的缩短。细胞内记录显示兴奋性突触后电位增加,尽管增加幅度小于细胞外场兴奋性突触后电位且不太规则。4. 对未强直刺激的输入通路进行刺激时,场电位反应以及细胞内测量的胞体膜电位、电阻或兴奋性均未出现相应变化。后两者的特性通过细胞内注入电流脉冲来测量。得出的结论是,长时程增强是特定于接受强直刺激的通路的。5. 强直刺激后还存在一个短时程(通常为2 - 4分钟)的抑制,最常出现在对照通路中,但有时在强直刺激侧也可见,叠加在增强之上。得出的结论是,短时程抑制并不局限于任何特定通路,而是一种普遍的(非特异性的)现象。

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