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CA1锥体细胞的基底突触和顶端突触采用不同的长时程增强诱导机制。

Basal and apical synapses of CA1 pyramidal cells employ different LTP induction mechanisms.

作者信息

Haley J E, Schaible E, Pavlidis P, Murdock A, Madison D V

机构信息

Department of Molecular and Cellular Physiology, Stanford University School of Medicine, California 94305, USA.

出版信息

Learn Mem. 1996 Nov-Dec;3(4):289-95. doi: 10.1101/lm.3.4.289.

Abstract

Nitric oxide (NO) production has been widely reported to be required for the induction of long-term potentiation (LTP) in hippocampal CA1 cells. Of the two constitutive isoforms of NO synthase, the endothelial form (eNOS) has been implicated in the induction of LTP in these cells. The distribution of eNOS within CA1 cells is not uniform, however, being present in the cell bodies and apical dendrites but absent from the basal dendrites. Using extracellular and intracellular recording techniques, we demonstrate that LTP induction in stratum radiatum synapses (onto apical dendrites) is dependent on NO production, being attenuated by pretreatment with a NOS inhibitor. LTP induced in stratum oriens synapses (onto basal dendrites) is, however, resistant to NOS inhibitors. Both forms of LTP require the activation of N-methyl-D-aspartate (NMDA) receptors because induction of LTP in both stratum radiatum and stratum oriens is blocked by AP5. Thus, it appears that synapses onto apical and basal dendrites of CA1 cells use different cellular mechanisms of LTP induction.

摘要

一氧化氮(NO)的产生被广泛报道为海马CA1细胞中诱导长时程增强(LTP)所必需。在两种组成型一氧化氮合酶同工型中,内皮型(eNOS)被认为与这些细胞中LTP的诱导有关。然而,eNOS在CA1细胞内的分布并不均匀,存在于细胞体和顶端树突中,但在基底树突中不存在。使用细胞外和细胞内记录技术,我们证明辐射层突触(至顶端树突)中的LTP诱导依赖于NO的产生,用一氧化氮合酶抑制剂预处理可使其减弱。然而,在原层突触(至基底树突)中诱导的LTP对一氧化氮合酶抑制剂具有抗性。两种形式的LTP都需要N-甲基-D-天冬氨酸(NMDA)受体的激活,因为辐射层和原层中LTP的诱导都被AP5阻断。因此,似乎CA1细胞顶端和基底树突上的突触使用不同的LTP诱导细胞机制。

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