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海马体CA3神经元中多种形式的长时程增强作用使用共同的突触后机制。

Multiple forms of LTP in hippocampal CA3 neurons use a common postsynaptic mechanism.

作者信息

Yeckel M F, Kapur A, Johnston D

机构信息

Division of Neuroscience, Baylor College of Medicine, Houston, Texas 77030, USA.

出版信息

Nat Neurosci. 1999 Jul;2(7):625-33. doi: 10.1038/10180.

Abstract

We investigated long-term potentiation (LTP) at mossy fiber synapses on CA3 pyramidal neurons in the hippocampus. Using Ca2+ imaging techniques, we show here that when postsynaptic Ca2+ was sufficiently buffered so that [Ca2+]i did not rise during synaptic stimulation, the induction of mossy fiber LTP was prevented. In addition, induction of mossy fiber LTP was suppressed by postsynaptic injection of a peptide inhibitor of cAMP-dependent protein kinase. Finally, when ionotropic glutamate receptors were blocked, LTP depended on the postsynaptic release of Ca2+ from internal stores triggered by activation of metabotropic glutamate receptors. These results support the conclusion that mossy fiber LTP and LTP at other hippocampal synapses share a common induction mechanism involving an initial rise in postsynaptic [Ca2+].

摘要

我们研究了海马体中CA3锥体神经元上苔藓纤维突触的长时程增强(LTP)。使用钙离子成像技术,我们在此表明,当突触后钙离子得到充分缓冲,使得在突触刺激期间细胞内钙离子浓度([Ca2+]i)不升高时,苔藓纤维LTP的诱导就会被阻止。此外,通过突触后注射一种环磷酸腺苷(cAMP)依赖性蛋白激酶的肽抑制剂,苔藓纤维LTP的诱导受到抑制。最后,当离子型谷氨酸受体被阻断时,LTP依赖于代谢型谷氨酸受体激活引发的细胞内钙库中钙离子的突触后释放。这些结果支持了这样一个结论,即苔藓纤维LTP与海马体其他突触处的LTP共享一种涉及突触后[Ca2+]初始升高的共同诱导机制。

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