Intracellular calcium ion dynamics involved in long-term potentiation in hippocampal CA1 neurons in mice lacking the IP₃ type 1 receptor

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• 作者：Masatomo Yoshioka ; Yoshihiko Yamazaki ; Satoshi Fujii ; Kenya Kaneko ; Hiroshi Kato ; Katsuhiko Mikoshiba
• 关键词：Intracellular calcium ion ; Long-term potentiation ; Hippocampus ; Inositol-1 ; 4 ; 5-trisphosphate ; Knockout mouse ; Ca²⁺ imaging
• 刊名：Neuroscience Research
• 出版年：2010
• 出版时间：June 2010
• 年：2010
• 卷：67
• 期：2
• 页码：149-155
• 全文大小：657 K

文摘

In the present study, mice lacking the type 1 inositol-1,4,5-trisphosphate receptor (IP₃R) were used to study the role of type 1 IP₃Rs in the induction of long-term potentiation (LTP) in hippocampal CA1 neurons. The magnitude of the LTP induced by high frequency stimulation (HFS) consisting of 20 pulses at 30 Hz in mice lacking type 1 IP₃Rs was significantly larger than that in wild-type mice in terms of the field excitatory postsynaptic potential and population spike. By measuring changes in the intracellular Ca²⁺ concentration ([Ca²⁺]_i) in CA1 pyramidal neurons using fluorometry, we found that the decay time of the transient increase in the [Ca²⁺]_i evoked by the HFS in mutant mice was significantly longer than that in wild-type mice, whereas the [Ca²⁺]_i at rest and the magnitude of the [Ca²⁺]_i increases caused by the HFS were no different from those in wild-type mice. In slices from the mutant mice, paired-pulse stimulation (PPS) delivered at an interval of 10 ms resulted in significantly weaker paired-pulse inhibition (PPI) than in wild-type mice, suggesting that lack of type 1 IP₃Rs reduces the PPI induced by PPS in the CA1 region. These results indicate that a lack of type 1 IP₃Rs causes a slower decay of the transient [Ca²⁺]_i in CA1 pyramidal neurons and attenuates the activity of inhibitory interneurons, resulting in enhancement of LTP induction.