Postsynaptic control of hippocampal long-term potentiation.
Postsynaptic control of hippocampal long-term potentiation.
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发表时间：
1986
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通讯作者：
H. Wigström;B. Gustafsson
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作者：
H. Wigström;B. Gustafsson
海马中的长时程增强（LTP）具有协同性的特性，即如果大量的传入纤维被强直化，则产生更大的增强。突触后机制在这一过程中的可能参与进行了研究，在CA 1区的海马切片制备。GABA拮抗剂如印防己毒素阻断突触后抑制后，LTP的诱导大大促进。在印防己毒素处理的切片，LTP诱导的单齐射刺激的途径，如果这些发生在与其他传入短暂强直激活。这种相互作用在很短的时间内（小于50毫秒），也存在，如果输入在空间上分开（输入到基底和顶端树突之间的协同性）。LTP可以诱导配对单齐射突触激活和胞内注射去极化电流脉冲，时间要求是类似于在细胞外的“连接研究”中观察到的。先前的研究表明，N-甲基-D-天冬氨酸（NMDA）型谷氨酸受体通道在某种程度上参与了LTP诱导。这里提供的证据表明，导致LTP的激活会引发对NMDA受体阻滞剂2-氨基-5-磷酸戊酸（APV）敏感的电位，表明电流通过NMDA受体通道。结果表明，海马LTP依赖于同时的突触前递质释放和突触后去极化，其方式类似于HEBB（1949）提出的联想学习模型。此外，有人提出，所需的突触前和突触后的相互作用是由NMDA受体通道复合物，这是已知的具有所需的电压和发射器的灵敏度。（250字处删节）
Long-term potentiation (LTP) in the hippocampus has the property of cooperativity, i.e. greater potentiation is produced if a larger number of afferent fibres is tetanized. The possible involvement of postsynaptic mechanisms in this process was investigated in the CA1 area of the hippocampal slice preparation. Following blockade of postsynaptic inhibition by GABA antagonists, e.g. picrotoxin, the induction of LTP was greatly facilitated. In picrotoxin-treated slices, LTP was induced in a pathway stimulated by single volleys, if these occurred in conjunction with brief tetanic activation of other afferents. This interaction operated over a short period of time (less than 50 ms) and was also present if the inputs were separated in space (cooperativity between inputs to basal and apical dendrites). LTP could be induced by pairing single volley synaptic activation and intracellularly injected depolarizing current pulses, the timing requirements being similar to those observed in the extracellular "conjunction studies". Previous studies have suggested that glutamate receptor channels of the N-methyl-D-aspartate (NMDA) type are somehow involved in LTP induction. Evidence presented here shows that activation leading to LTP evokes a potential which is sensitive to the NMDA receptor blocker 2-amino-5-phosphonovalerate (APV), indicating passage of current through NMDA receptor channels. The results suggest that hippocampal LTP depends on simultaneous presynaptic transmitter release and postsynaptic depolarization in a manner analogous to the model proposed by HEBB (1949) for associative learning. Furthermore, it is proposed that the required pre- and postsynaptic interaction is handled by the NMDA receptor channel complex, which is known to have the required voltage and transmitter sensitivity.(ABSTRACT TRUNCATED AT 250 WORDS)