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γ-氨基丁酸能抑制对慢性制备大鼠新皮质长时程增强的影响。

Effects of GABAergic inhibition on neocortical long-term potentiation in the chronically prepared rat.

作者信息

Komaki Alireza, Shahidi Siamak, Lashgari Reza, Haghparast Abbas, Malakouti S Mansour, Noorbakhsh S Mohammad

机构信息

Department of Physiology, School of Medicine, Hamedan University of Medical Sciences, Hamedan, Iran.

出版信息

Neurosci Lett. 2007 Jul 18;422(3):181-6. doi: 10.1016/j.neulet.2007.06.017. Epub 2007 Jun 17.

Abstract

Long-term potentiation (LTP) is a form of activity-dependent synaptic plasticity that is a candidate cellular mechanism for some forms of learning and memory. Although GABAergic synaptic inhibition plays a critical role in regulating of synaptic plasticity, there is still little known about the GABAergic modulation on LTP induction in chronic preparation. In the present study we examined the effect of GABA(A) agonist, diazepam (DZM), and antagonist, picrotoxin (PTX) on the induction of LTP in the somatosensory cortex of freely moving rats for a long-term period. In adult rats a bipolar stimulating and recording electrode were implanted into corpus callusom and somatosensory cortex, respectively. Two weeks after the surgery, evoked field potential responses were recorded before, during (12 days), and after (1 month) induction period of LTP by high-frequency stimulation. The LTP characteristics were compared between control, DZM and PTX groups during the time course of recording in each rat. Administration of DZM prior to train, blocked the induction of neocortical LTP, while the PTX increased the development of LTP making the highest differential levels of LTP about 12 days after the initiation of LTP induction. Our findings suggest that the augmentation of LTP by PTX can be explained by an interaction between excitatory and inhibitory pathways. Suppression of neocortical inhibitory inputs by PTX causes enhancement in LTP induction. These results suggest that GABAergic system has an important role in synaptic plasticity and long-term modification of somatosensory cortex in freely moving rat.

摘要

长时程增强(LTP)是一种依赖活动的突触可塑性形式,是某些形式学习和记忆的潜在细胞机制。尽管γ-氨基丁酸(GABA)能突触抑制在调节突触可塑性中起关键作用,但关于慢性制备中GABA能对LTP诱导的调制仍知之甚少。在本研究中,我们长期检测了GABA(A)激动剂地西泮(DZM)和拮抗剂印防己毒素(PTX)对自由活动大鼠体感皮层LTP诱导的影响。在成年大鼠中,分别将双极刺激和记录电极植入胼胝体和体感皮层。手术后两周,在高频刺激诱导LTP的前、中(12天)、后(1个月)记录诱发场电位反应。在每只大鼠记录的时间过程中,比较对照组、DZM组和PTX组的LTP特征。训练前给予DZM可阻断新皮层LTP的诱导,而PTX则增强LTP的发展,使LTP诱导开始后约12天的LTP差异水平最高。我们的研究结果表明,PTX对LTP的增强作用可通过兴奋性和抑制性通路之间的相互作用来解释。PTX对新皮层抑制性输入的抑制导致LTP诱导增强。这些结果表明,GABA能系统在自由活动大鼠的突触可塑性和体感皮层的长期修饰中起重要作用。

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