Low-frequency stimulation erases LTP through an NMDA receptor-mediated activation of protein phosphatases.
Low-frequency stimulation erases LTP through an NMDA receptor-mediated activation of protein phosphatases.
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DOI：
10.1101/lm.1.2.129
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发表时间：
1994-07
影响因子：
2
通讯作者：
T. O’Dell;E. Kandel
中科院分区：
文献类型：
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作者：
T. O’Dell;E. Kandel
在成年豚鼠海马CA1区，长序列的θ频率（5 Hz）刺激对基础突触传递有微弱的增强作用，但抑制了最近经历了长期增强（LTP）的突触的突触传递强度。在高频刺激之前立即进行的5赫兹刺激也抑制了随后的LTP诱导。5hz刺激对增强突触的抑制（去增强）被2-氨基-5-磷酸戊酸阻断，并且仅在LTP的早期阶段观察到。此外，蛋白磷酸酶抑制剂冈田酸和calyculin A阻断了5hz刺激的去增强和抑制后续LTP的能力，这表明蛋白磷酸酶参与了5hz刺激调节海马CA1区突触可塑性的能力。
In the CA1 region of adult guinea pig hippocampal slices, long trains of theta frequency (5 Hz) stimulation produced a small enhancement of basal synaptic transmission but depressed the strength of synaptic transmission at synapses that had recently undergone long-term potentiation (LTP). Five hertz stimulation delivered immediately prior to high-frequency stimulation also inhibited the subsequent induction of LTP. The depression of potentiated synapses by 5 Hz stimulation (depotentiation) was blocked by 2-amino-5-phosphonovalerate and was observed only during the early phases of LTP. Furthermore, the protein phosphatase inhibitors okadaic acid and calyculin A blocked both depotentiation and the ability of 5 Hz stimulation to inhibit subsequent LTP, suggesting that protein phosphatases are involved in the ability of 5 Hz stimulation to modulate synaptic plasticity in the CA1 region of the hippocampus.