Facilitation of low-frequency stimulation-induced long-term potentiation by endogenous noradrenaline and serotonin in developing rat visual cortex
Facilitation of low-frequency stimulation-induced long-term potentiation by endogenous noradrenaline and serotonin in developing rat visual cortex
复制标题
DOI：
10.1016/j.neures.2009.02.014
复制
发表时间：
2009-06-01
影响因子：
2.9
通讯作者：
Komatsu, Yukio
中科院分区：
文献类型：
--
作者：
Inaba, Mie;Maruyama, Takuro;Komatsu, Yukio
T型钙通道依赖性长时程增强（LTP）主要发生在大鼠和猫视皮层眼优势可塑性的关键期。已知去甲肾上腺素和血清素促进眼优势可塑性。在这项研究中，使用大鼠的视觉皮层切片，我们测试是否这种LTP是由这些神经调节剂以同样的方式调节眼优势可塑性。记录从层2/3和LTP诱导的低频（2 Hz）刺激持续15 min的层4刺激诱发的细胞外场电位。LTP的诱导被抑制β，但不是α，肾上腺素能受体拮抗剂。5-HT 1A或5-HT 2受体的选择性拮抗剂也抑制LTP诱导。在制备的大鼠脑片中，去甲肾上腺素或5-羟色胺被选择性神经毒素耗尽，LTP的幅度显着小于控制切片。这些结果表明，相同类型的肾上腺素能和肾上腺素能受体促进LTP和眼优势可塑性，支持我们的假设，T型钙通道依赖的LTP介导的关键期皮层神经元的视觉反应的经验依赖性增强。(C)2009年爱思唯尔爱尔兰有限公司和日本神经科学学会。All rights reserved.
T-type Ca2+ channel-dependent long-term potentiation (LTP) occurs predominantly during the critical period of ocular dominance plasticity in rat and cat visual cortex. Noradrenaline and serotonin are known to facilitate ocular dominance plasticity. In this study using rat visual cortical slices, we tested whether this LTP is modulated by these neuromodulators in the same way as ocular dominance plasticity. Extracellular field potentials evoked by layer 4 stimulation were recorded from layer 2/3 and LTP was induced by low-frequency (2 Hz) stimulation continued for 15 min. The induction of LTP was suppressed by beta, but not alpha, adrenergic receptor antagonists. LTP induction was also inhibited by selective antagonists for 5-HT1A or 5-HT2 receptors. In slices prepared from rats in which noradrenaline or serotonin was depleted by selective neurotoxins, the magnitude of LTP was significantly smaller compared with control slices. These results indicate that the same types of adrenergic and serotonergic receptors facilitate both LTP and ocular dominance plasticity, supporting our hypothesis that T-type Ca2+ channel-dependent LTP mediates experience-dependent enhancement of visual responses of cortical neurons during the critical period. (C) 2009 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.