Substrates for coincidence detection and calcium signaling for induction of synaptic potentiation in the neonatal visual cortex.-猫眼课题宝

用于一致性检测和钙信号传导的底物，用于诱导新生儿视觉皮层的突触增强。

DOI：

10.1152/jn.00908.2003

发表时间：

2004

期刊：

Journal of neurophysiology.

影响因子：

通讯作者：

中科院分区：

文献类型：

作者：

Schrader,LauraA;Perrett,StephenP;Ye,Lan;Friedlander,MichaelJ

Regulation of the efficacy of synaptic transmission by activity-dependent processes has been implicated in learning and memory as well as in developmental processes. We previously described transient potentiation of excitatory synapses onto layer 2/3 pyramidal neurons in the visual cortex that is induced by coincident presynaptic stimulation and postsynaptic depolarization. In the adult visual cortex, activation ofN-methyl-d-aspartate (NMDA) glutamate receptors is necessary to induce this plasticity. These receptors act as coincidence detectors, sensing presynaptic glutamate release and postsynaptic depolarization, and cause an influx of Ca2+that is necessary for the potentiation. In the neurons of the neonatal visual cortex, on the other hand, coincident presynaptic stimulation and postsynaptic depolarization induce stable long-term potentiation (LTP). In addition, reduced but significant LTP can be induced in many neurons in the presence of the NMDA receptor (NMDAR) antagonist, 2-amino-5-phosphonovaleric acid despite the Ca2+requirement. Therefore there must be an alternative postsynaptic Ca2+source and coincidence detection mechanism linked to the LTP induction mechanism in the neonatal cortex operating in addition to NMDARs. In this study, we find that in layer 2/3 pyramidal neurons, release of Ca2+from inositol trisphosphate (InsP3) receptor-mediated intracellular stores and influx through voltage-gated Ca2+channels (VGCCs) provide alternative postsynaptic Ca2+sources. We hypothesize that InsP3Rs are coincidence detectors, sensing presynaptic glutamate release through linkage with group I metabotropic glutamate receptors (mGluRs), and depolarization, through VGCCs. We also find that the downstream protein kinases, PKA and PKC, have a role in potentiation in layer 2/3 pyramidal neurons of the neonatal visual cortex.