Presynaptic inhibition of the monosynaptic reflex pathway in kittens
Presynaptic inhibition of the monosynaptic reflex pathway in kittens
复制标题
小猫单突触反射通路的突触前抑制
DOI：
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发表时间：
1963
期刊：
影响因子：
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通讯作者：
W. Willis
中科院分区：
文献类型：
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作者：
R. Eccles;W. Willis
马尔科姆(Malcolm，1955)和斯科格伦德(Skoglund，1960a)最近对猫的腰骶髓突触传递的研究发现，肌肉神经的一次条件性抽射对单突触反射的抑制非常持久，这种抑制可持续约100毫秒，并持续长达800毫秒。Skoglund发现，当屈肌神经的传入抽动对由伸神经抽动引起的单突触反射产生条件性单突触反射时，这种抑制延长，但反向组合只有短暂的抑制，其他组合显然没有被研究。在成年猫屈肌神经中的条件性抽动被证明在数百毫秒的时间内减少了从运动神经元记录的单突触兴奋性突触后电位(EPSP)，而不会对突触后膜的性质产生任何改变(Frank&Fuortes，1957；Frank，1959；Eccle，Eccle&Magni，1961)。EPSP的抑制导致单突触反射的减少(Eccle，Schmidt&Willis，1962a)。EPSP抑制与第一类初级传入纤维的去极化之间的精确关联(Eccle，Magni&Willis，1962)导致了EPSP抑制是由初级传入去极化引起的假说(Eccle，Eccle&Magni，1961；Eccle，1961a，b)。有充分的证据表明，神经末梢的去极化将减少突触前神经冲动释放的递质物质的数量(Hagiwara&Tasaki，1958；Hubbard&Willis，1962；Eccle，Kostiuk&Schmidt，1962c；Takeuchi&Takeuchi，1962)，现在有组织学证据表明，在中枢神经系统的不同部分存在特殊突触与其他突触终末的关系(Kidd，1962；Gray，1962；a，b；Szentagothai，个人交流)。因此，似乎可以肯定的是，EPSP抑郁是由突触前作用的抑制过程引起的。
In recent studies on synaptic transmission in the lumbosacral spinal cord of kittens, Malcolm (1955) and Skoglund (1960a) found that a single conditioning volley in a muscle nerve produced a very prolonged inhibition of monosynaptic reflexes, which was complete for about 100 msec and persisted for as long as 800 msec. Skoglund found this prolonged inhibition when afferent volleys in flexor nerves conditioned monosynaptic reflexes which were evoked by volleys in extensor nerves, but there was only a brief inhibition with the reverse combination, and other combinations apparently were not investigated. Conditioning volleys in flexor nerves of adult cats have been shown to reduce the monosynaptic excitatory post-synaptic potential (EPSP) recorded from motoneurones for a period of hundreds of milliseconds without producing any change in the post-synaptic membrane properties (Frank & Fuortes, 1957; Frank, 1959; Eccles, Eccles & Magni, 1961). The depression of the EPSP results in a reduction of the monosynaptic reflex (Eccles, Schmidt & Willis, 1962a). A precise correlation between EPSP depression and a depolarization of Group I a primary afferent fibres (Eccles, Magni & Willis, 1962) has led to the hypothesis that the EPSP depression is caused by the primary afferent depolarization (Eccles, Eccles & Magni, 1961; Eccles, 1961 a, b). There is ample evidence that a depolarization of nerve terminals will reduce the amount of transmitter substance released by presynaptic nerve impulses (Hagiwara & Tasaki, 1958; Hubbard & Willis, 1962; Eccles, Kostyuk & Schmidt, 1962c; Takeuchi & Takeuchi, 1962), and there is now histological evidence that special synapses exist in relationship to other synaptic endings in various parts of the central nervous system (Kidd, 1962; Gray, 1962; a, b; Szentagothai, personal communication). Therefore, it seems certain that the EPSP depression is caused by an inhibitory process which acts presynaptically.