Synaptic plasticity in hippocampal CA1 neurons of mice lacking type 1 inositol-1,4,5-trisphosphate receptors
Synaptic plasticity in hippocampal CA1 neurons of mice lacking type 1 inositol-1,4,5-trisphosphate receptors
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DOI：
10.1101/lm.34100
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发表时间：
2000-09-01
影响因子：
2
通讯作者：
Mikoshiba, K
中科院分区：
文献类型：
--
作者：
Fujii, S;Matsumoto, M;Mikoshiba, K
在野生型小鼠的海马CA 1神经元中，递送标准破伤风毒素（100 Hz的100个脉冲）或一系列低频刺激（LFS; 1000个脉冲（1 Hz）分别诱导反应的长时程增强（LTP）或长时程抑制（LTD），破伤风后60分钟传递LFS导致LTP逆转（去增强作用，DP），而在破伤风前10分钟应用的LFS抑制LTP诱导（LTP抑制）。为了评估1型肌醇-1，4，5-三磷酸受体（IP 3R 1）在海马突触可塑性中的作用，我们研究了缺乏IP 3R 1的小鼠CA 1神经元中的场兴奋性突触后电位（EPSP）的LTP、LTD、DP和LTP抑制。在由标准破伤风或LFS诱导的LTP或LTD的平均幅度方面，突变型小鼠和野生型小鼠之间未见差异。然而，短破伤风（100赫兹100脉冲）诱导的LTP的平均幅度显着大于突变型小鼠比野生型小鼠。此外，DP或LTP抑制减弱突变小鼠，平均幅度的响应后，交付LFS或破伤风显着大于野生型小鼠。这些结果表明，在海马CA 1区神经元，IP 3R 1参与LTP，DP和LTP抑制，但不是必需的LTD。在缺乏IP 3R 1的小鼠中观察到的LTP诱导和DP和LTP抑制衰减的促进表明，该受体在阻断海马CAI神经元的突触增强中起着重要作用。
In hippocampal CA1 neurons of wild-type mice, delivery of a standard tetanus (100 pulses at 100 Hz) or a train of low-frequency stimuli (LFS; 1000 pulses at I Hz) to a naive input pathway induces, respectively, long-term potentiation (LTP) or long-term depression (LTD) of responses, and delivery of LFS 60 min after tetanus results in reversal of LTP (depotentiation, DP), while LFS applied GO min before tetanus suppresses LTP induction (LTP suppression). To evaluate the role of the type 1 inositol-1,4,5-trisphosphate receptor (IP3R1) in hippocampal synaptic plasticity, we studied LTP, LTD, DP, and LTP suppression of the field excitatory postsynaptic potentials (EPSPs) in the CA1 neurons of mice lacking the IP3R1. No differences were seen between mutant and wild-type mice in terms of the mean magnitude of the LTP or LTD induced by a standard tetanus or LFS. However, the mean magnitude of the LTP induced by a short tetanus (100 pulses at 100 Hz) was significantly greater in mutant mice than in wild-type mice. In addition, DP or LTP suppression was attenuated in the mutant mice, the mean magnitude of the responses after delivery of LFS or tetanus being significantly greater than in wild-type mice. These results suggest that, in hippocampal CA1 neurons, the IP3R1 is involved in LTP, DP, and LTP suppression but is not essential for LTD. The facilitation of LTP induction and attenuation of DP and LTP suppression seen in mice lacking the IP3R1 indicates that this receptor plays an important role in blocking synaptic potentiation in hippocampal CAI neurons.