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评估不同的诱导方案以在体内诱导大鼠视觉皮层的长时程压抑(LTD)。

Assessment of different induction protocols to elicit long-term depression (LTD) in the rat visual cortex in vivo.

机构信息

Department of Psychology, Kingston, Ontario, Canada K7L 3N6.

出版信息

Brain Res. 2010 Mar 8;1318:33-41. doi: 10.1016/j.brainres.2009.12.063. Epub 2010 Jan 4.

DOI:10.1016/j.brainres.2009.12.063
PMID:20051240
Abstract

Changes in synaptic efficacy, including long-term potentiation (LTP) and long-term depression (LTD), provide mechanisms for experience-induced plasticity of cortical and subcortical circuits. LTP is readily induced under drastically different experimental conditions (e.g., in vitro and in vivo). However, few studies have compared the effectiveness of different induction protocols to elicit synaptic depression, especially under in vivo conditions. Here, we assessed the effectiveness of four different low frequency stimulation (LFS) protocols, applied to the lateral geniculate nucleus, to induce LTD-like changes of local field postsynaptic potentials (fPSPs) recorded on the surface of the primary visual cortex (V1) of urethane-anesthetized rats. Three LFS protocols (900 pulses at 1 Hz; 1800 pulses at 1 Hz, 1800 pulses at 1 Hz, repeated three times), known to induce LTD in neocortical and hippocampal slice preparations, failed to induce synaptic depression. In contrast, strong low frequency burst stimulation (3 pulses/burst at 20 Hz, 900 bursts repeated at 1 Hz) resulted in significant, but transient ( approximately 20 min) depression of fPSPs in V1. This effect was resistant to systemic treatment with MK 801 (0.5 mg/kg) or local, cortical application of either APV (10 mM) or MCPG (10 mM), indicative of non-essential roles of N-methyl-d-aspartate and metabotropic glutamate receptors. A similar depressant effect was also observed under sodium pentobarbital anesthesia. These experiments emphasize the resistance of the in vivo neocortex to express the long-lasting down-regulation of synaptic strength, observations that require integration into current models and theories regarding the functions of LTD as a homeostatic and experience-dependent plasticity mechanism.

摘要

突触效能的变化,包括长时程增强(LTP)和长时程抑制(LTD),为皮质和皮质下回路的经验依赖性可塑性提供了机制。LTP 在截然不同的实验条件下很容易被诱导(例如,在体外和体内)。然而,很少有研究比较不同诱导方案引发突触抑制的有效性,特别是在体内条件下。在这里,我们评估了四种不同的低频刺激(LFS)方案在 lateral geniculate nucleus 中的有效性,以诱导局部场突触后电位(fPSPs)在 urethane 麻醉大鼠初级视觉皮层(V1)表面记录的类似 LTD 的变化。三种 LFS 方案(900 个脉冲,1Hz;1800 个脉冲,1Hz,重复三次),已知可诱导新皮层和海马切片制备中的 LTD,未能诱导突触抑制。相比之下,强烈的低频脉冲刺激(20Hz 时 3 个脉冲/脉冲,1Hz 时重复 900 个脉冲)导致 V1 中的 fPSPs 显著但短暂(约 20 分钟)抑制。这种效应对全身给予 MK 801(0.5mg/kg)或局部给予 APV(10mM)或 MCPG(10mM)均有抗性,表明 N-甲基-D-天冬氨酸和代谢型谷氨酸受体的非必需作用。在戊巴比妥钠麻醉下也观察到类似的抑制作用。这些实验强调了体内新皮层抵抗表达突触强度持久下调的能力,这些观察结果需要整合到当前关于 LTD 作为一种平衡和经验依赖性可塑性机制的功能的模型和理论中。

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