Role of P2X4 receptors in synaptic strengthening in mouse CA1 hippocampal neurons.
Role of P2X4 receptors in synaptic strengthening in mouse CA1 hippocampal neurons.
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DOI：
10.1111/j.1460-9568.2011.07763.x
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发表时间：
2011-07
期刊：
影响因子：
--
通讯作者：
North RA
中科院分区：
文献类型：
--
作者：
Baxter AW;Choi SJ;Sim JA;North RA
P2 X4受体是由细胞外ATP门控的钙渗透性阳离子通道。它们被发现接近海马CA 1神经元上的突触下位点。我们比较了野生型和P2 X4基因敲除小鼠（21-26日龄）之间突触强化的特征。强直性突触前刺激（100 Hz，1 s）与突触后去极化配对诱发的增强在P2 X4 −/−小鼠中比野生型小鼠少（230 vs. 50%增强）。配对脉冲比和自发兴奋性突触后电流（EPSC）的幅度和频率在野生型和基因敲除小鼠之间没有差异。先前的超极化（10个3 s脉冲至-120 mV，0.17 Hz）增强了野生型小鼠自发EPSC的幅度，但在P2 X4 −/−小鼠中没有;这种增强不受硝苯地平的影响，但被记录移液管中的10 mm 1，2-双（邻氨基苯氧基）乙烷-N，N，N′，N′-四乙酸（BAPTA）消除。N-甲基-d-天冬氨酸EPSC（6-氰基-7-硝基喹喔啉-2，3-二酮，10或30 μm，−100 mV）的振幅在无镁溶液中记录20分钟时得到促进。在野生型小鼠中，细胞内BAPTA（10 mm）、艾芬地尔（3 μm）或4-（4-氟苯基）-2-（4-甲基亚磺酰基苯基）-5-（4-吡啶基）1H-咪唑（5 μm）可使N-甲基-d-天冬氨酸EPSC的这种促进作用降低约50%。在P2 X4 −/−小鼠中，这种促进作用要小得多，并且不受细胞内BAPTA、艾芬地尔（3 μm）或促分裂原活化蛋白（MAP）激酶抑制剂4-（4-氟苯基）-2-（4-甲基亚磺酰基苯基）-5-（4-吡啶基）1H-咪唑（5 μm）的影响。这表明，P2 X4受体的缺乏限制了NR 2B亚基掺入突触N-甲基-d-天冬氨酸受体。
P2X4 receptors are calcium-permeable cation channels gated by extracellular ATP. They are found close to subsynaptic sites on hippocampal CA1 neurons. We compared features of synaptic strengthening between wild-type and P2X4 knockout mice (21–26 days old). Potentiation evoked by a tetanic presynaptic stimulus (100 Hz, 1 s) paired with postsynaptic depolarization was less in P2X4−/− mice than in wild-type mice (230 vs. 50% potentiation). Paired-pulse ratios and the amplitude and frequency of spontaneous excitatory postsynaptic currents (EPSCs) were not different between wild-type and knockout mice. Prior hyperpolarization (ten 3 s pulses to −120 mV at 0.17 Hz) potentiated the amplitude of spontaneous EPSCs in wild-type mice, but not in P2X4−/− mice; this potentiation was not affected by nifedipine, but was abolished by 10 mm 1,2-bis(o-aminophenoxy)ethane-N,N,N′,N′-tetra-acetic acid (BAPTA) in the recording pipette. The amplitude of N-methyl-d-aspartate EPSCs (in 6-cyano-7-nitroquinoxaline-2,3-dione, 10 or 30 μm, at −100 mV) facilitated during 20 min recording in magnesium-free solution. In wild-type mice, this facilitation of the N-methyl-d-aspartate EPSC was reduced by about 50% by intracellular BAPTA (10 mm), ifenprodil (3 μm) or 4-(4-fluorophenyl)-2-(4-methylsulphinylphenyl)-5-(4-pyridyl)1H-imidazole (5 μm). In P2X4−/− mice, the facilitation was much less, and was unaffected by intracellular BAPTA, ifenprodil (3 μm) or mitogen-activated protein (MAP) kinase inhibitor 4-(4-fluorophenyl)-2-(4-methylsulphinylphenyl)-5-(4-pyridyl)1H-imidazole (5 μm). This suggests that the absence of P2X4 receptors limits the incorporation of NR2B subunits into synaptic N-methyl-d-aspartate receptors.
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