Presynaptic activity and Ca2+ entry are required for the maintenance of NMDA receptor-independent LTP at visual cortical excitatory synapses
Presynaptic activity and Ca2+ entry are required for the maintenance of NMDA receptor-independent LTP at visual cortical excitatory synapses
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DOI：
10.1152/jn.00602.2003
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发表时间：
2004-08-01
影响因子：
2.5
通讯作者：
Komatsu, Y
中科院分区：
文献类型：
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作者：
Liu, HN;Kurotani, T;Komatsu, Y
我们已经证明一些神经活动是维持视觉皮层抑制性突触的长期增强（LTP）所必需的。我们测试了在发育中的大鼠视觉皮层2/3层细胞中n -甲基- d -天冬氨酸（NMDA）受体独立的兴奋性连接LTP中是否也存在这种情况。这种LTP在施加2 Hz刺激15分钟后发生，并且在0.1 Hz的测试刺激继续时持续数小时。当LTP诱导后1小时停止测试刺激时，只有三分之一的LTP实例消失，但在药物抑制自发放电的情况下，大多数LTP实例消失，这表明LTP维持需要诱发或自发活动。LTP被利多卡因暂时阻断动作电位或LTP诱导后去除细胞外Ca2+完全消除，但在突触后细胞的电压钳或谷氨酸受体拮抗剂kynurenate暂时阻断突触后活性后，LTP仍然存在，这表明LTP的维持需要突触前，而不是突触后，放电和Ca2+进入。在药物阻断p型Ca2+通道后，超过一半的LTP实例被消除，而在l型或Ni2+敏感的Ca2+通道阻断后，LTP实例持续存在。这些结果表明，维持NMDA受体独立的兴奋性LTP需要突触前放电和Ca2+通道激活作为抑制性LTP，尽管前者的放电和Ca2+进入的必要水平似乎低于后者，并且所涉及的Ca2+通道类型只是部分相同。
We have shown that some neural activity is required for the maintenance of long-term potentiation (LTP) at visual cortical inhibitory synapses. We tested whether this was also the case in N-methyl-D-aspartate (NMDA) receptor-independent LTP of excitatory connections in layer 2/3 cells of developing rat visual cortex. This LTP occurred after 2-Hz stimulation was applied for 15 min and always persisted for several hours while test stimulation was continued at 0.1 Hz. When test stimulation was stopped for 1 h after LTP induction, only one-third of the LTP instances disappeared, but most did disappear under a pharmacological suppression of spontaneous firing, indicating that LTP maintenance requires either evoked or spontaneous activities. LTP was totally abolished by a temporary blockade of action potentials with lidocaine or the removal of extracellular Ca2+ after LTP induction, but it persisted under a voltage clamp of postsynaptic cells or after a temporary blockade of postsynaptic activity with the glutamate receptor antagonist kynurenate, suggesting that LTP maintenance requires presynaptic, but not postsynaptic, firing and Ca2+ entry. More than one-half of the LTP instances were abolished after a pharmacological blockade of P-type Ca2+ channels, whereas it persisted after either L-type or Ni2+-sensitive Ca2+ channel blockades. These results show that the maintenance of NMDA receptor-independent excitatory LTP requires presynaptic firing and Ca2+ channel activation as inhibitory LTP, although the necessary level of firing and Ca2+ entry seems lower for the former than the latter and the Ca2+ channel types involved are only partly the same.