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颞叶-海马CA1区突触传递的长期抑制

Long-term depression of temporoammonic-CA1 hippocampal synaptic transmission.

作者信息

Dvorak-Carbone H, Schuman E M

机构信息

Howard Hughes Medical Institute, Division of Biology 216-76, California Institute of Technology, Pasadena, California 91125, USA.

出版信息

J Neurophysiol. 1999 Mar;81(3):1036-44. doi: 10.1152/jn.1999.81.3.1036.

DOI:10.1152/jn.1999.81.3.1036
PMID:10085331
Abstract

The temporoammonic pathway, the direct projection from layer III of the entorhinal cortex to area CA1 of the hippocampus, includes both excitatory and inhibitory components that are positioned to be an important source of modulation of the hippocampal output. However, little is known about synaptic plasticity in this pathway. We used field recordings in hippocampal slices prepared from mature (6- to 8-wk old) rats to study long-term depression (LTD) in the temporoammonic pathway. Low-frequency (1 Hz) stimulation (LFS) for 10 min resulted in a depression of the field response that lasted for >/=1 h. This depression was saturable by multiple applications of LFS. LTD induction was unaffected by the blockade of either fast (GABAA) or slow (GABAB) inhibition. Temporoammonic LTD was inhibited by the presence of the N-methyl-D-aspartate (NMDA) receptor antagonist AP5, suggesting a dependence on calcium influx. Full recovery from depression could be induced by high-frequency (100 Hz) stimulation (HFS); in the presence of the GABAA antagonist bicuculline, HFS induced recovery above the original baseline level. Similarly, HFS or theta-burst stimulation (TBS) applied to naive slices caused little potentiation, whereas HFS or TBS applied in the presence of bicuculline resulted in significant potentiation of the temporoammonic response. Our results show that, unlike the Schaffer collateral input to CA1, the temporoammonic input in mature animals is easy to depress but difficult to potentiate.

摘要

颞叶-海马通路,即从内嗅皮层第III层直接投射至海马CA1区的通路,包含兴奋性和抑制性成分,这些成分是海马输出调制的重要来源。然而,关于该通路中的突触可塑性,人们了解甚少。我们利用从成年(6至8周龄)大鼠制备的海马脑片进行场电位记录,以研究颞叶-海马通路中的长时程抑制(LTD)。1赫兹(Hz)的低频刺激(LFS)持续10分钟可导致场电位反应降低,且持续时间≥1小时。多次施加LFS可使这种降低达到饱和。LTD的诱导不受快速(GABAA)或慢速(GABAB)抑制阻断的影响。N-甲基-D-天冬氨酸(NMDA)受体拮抗剂AP5可抑制颞叶-海马通路的LTD,提示其依赖于钙内流。高频(100 Hz)刺激(HFS)可诱导从抑制状态完全恢复;在存在GABAA拮抗剂荷包牡丹碱的情况下,HFS可诱导恢复至高于原始基线水平。同样,对未处理的脑片施加HFS或θ波爆发刺激(TBS)几乎不会引起增强,而在存在荷包牡丹碱的情况下施加HFS或TBS则会导致颞叶-海马反应显著增强。我们的结果表明,与CA1区的Schaffer侧支输入不同,成年动物的颞叶-海马输入易于抑制但难以增强。

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