An intracellular study of dendrodendritic inhibitory synapses on mitral cells in the rabbit olfactory bulb.

An intracellular study of dendrodendritic inhibitory synapses on mitral cells in the rabbit olfactory bulb.
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兔嗅球二尖瓣细胞树突状抑制突触的细胞内研究。

DOI:
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发表时间:
1978
期刊:
Journal of Physiology
影响因子:
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通讯作者:
S. Takagi
S. Takagi
中科院分区:
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文献类型:
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作者:
K. Mori;S. Takagi

文献摘要

被引文献

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1. 在兔嗅球中,在侧嗅道(l.o.t)刺激下,记录二尖瓣细胞和颗粒细胞层神经元的细胞内电位。2. 大多数二尖瓣细胞的记录显示,在反向尖峰后出现了大的(5 ~ 21 mV)和长时间的(60 ~ 650 msec) i.p.s.p.s。在细胞内施加的超极化电流逐渐增加时,这些脉冲的振幅减小,然后极性反转。它们伴随着二尖瓣细胞膜的显著和持久的(长达100毫秒)电导增加。3. 二尖瓣细胞的反向ipsps与原始的超极化ipsps具有完全不同的时间过程,这表明抑制突触广泛分布于体细胞和树突上。4. g.c.l细胞可以记录到E.p.s.p.s,其发作潜伏期比二尖瓣细胞的发作潜伏期短约0.6 ms。通过比较g.c.l细胞和二尖瓣细胞在不同的l.o.t.刺激条件下的E.p.s.p.s的行为表明,这些g.c.l细胞是介导二尖瓣细胞抑制的抑制性中间神经元。5. 这些结果支持了树突通路激活颗粒细胞和随后抑制二尖瓣细胞的假设。
1. In the rabbit olfactory bulb, intracellular potentials were recorded from mitral cells and from neurones in the granule cell layer (g.c.l.) following lateral olfactory tract (l.o.t.) stimulation. 2. Most recordings from mitral cells showed large (5‐21 mV) and prolonged (60‐650 msec) i.p.s.p.s subseuqent to the antidromic spikes. These i.p.s.p.s decreased in amplitude and then reversed in polarity by progressive increase in hyperpolarizing current applied intracellularly. They were accompanied by a prominent and long lasting (up to 100 msec) conductance increase of the mitral cell membrane. 3. Reversed i.p.s.p.s of mitral cells having quite different time courses from the original hyperpolarizing i.p.s.p.s suggest that the inhibitory synapses are widely distributed on the soma and dendrites. 4. E.p.s.p.s could be recorded from g.c.l. cells whose onset latency was approximately 0.6 msec shorter than that of mitral cell i.p.s.p.s. Comparison of the behaviour of e.p.s.p.s in g.c.l. cells and that of mitral cell i.p.s.p. under various conditions of l.o.t. stimulation suggests that these g.c.l. cells are the inhibitory interneurones mediating mitral cell inhibition. 5. The results support the hypothesis of dendrodentritic pathways for activation of granule cells and subsequent inhibition of mitral cells.