Mechanisms underlying control of developmental plasticity by glutamate receptros of NMDA type

突触功效的长时程增强（LTP）是哺乳动物脑中使用依赖性突触可塑性的众所周知的实例。特别是在发育中的视皮层，LTP被认为是视皮层神经元在出生后发育的“关键时期”的环境可修改性的基础。以前的研究表明，N-甲基-D-天冬氨酸（NMDA）型谷氨酸受体可能在LTP的诱导中起作用，Ca^2+通过NMDA受体连接的通道进入突触后部位可能触发LTP的诱导过程。然而，没有直接的实验数据支持这一假设在发育中的视觉皮层。因此，在本研究中，我们试图验证这一假设，并发现NMDA受体拮抗剂的应用阻断了LTP的诱导，进一步发现，在强直传入刺激后，视皮层神经元注射Ca^2+螯合剂导致兴奋性突触后电位（EPSP）的长时程抑制（LTD），在大多数测试的切片中，同时诱导非螯合细胞场电位的LTP。这些结果表明，强直性突触输入相关的突触后低浓度游离Ca^<22+>可能导致LTD，而通过激活的NMDA受体连接通道的Ca^<2+>升高可能导致LTP。

Long-term potentiation (LTP) of synaptic efficacy is a well known example of a use-dependent synaptic plasticity in the mammalian brain. In the developing visual cortex In particular, LTP is proposed as a basis of environmental modifiability of visual cortical neurons during a "critical period" of postnatal development. Previous studies suggested that glutamate receptors of N-methyl-D-aspartate (NMDA) type may play a role in induction of LTP and an entry of Ca^<2+> into postsynaptic sites through NMDA receptor-linked channels may trigger processes for induction of LTP. However, there were no direct experimental data supporting this hypothesis in the developing visual cortex. In the present study, therefore, we attempted to test this hypothesis and found that the induction of LTP is blocked by the application of an NMDA receptor antagonist and further that an injection of a Ca^<2+>-chelator into visual cortical neurons leads to long-term depression (LTD) of their excitatory postsynaptic potentials (EPSPs) following tetanic afferent stimuli which in most of the slices tested, simultaneously induce LTP of field potentials derived from unchelated cells. These results suggest that the low concentration of postsynaptic, free Ca^<22+> associated which tetanic synaptic inputs may lead to LTD while a rise of Ca^<2+> through activated NMDA receptor-linked channels may lead to LTP.