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大鼠视觉皮层中诱导突触长时程增强的 5-羟色胺能作用的发育性转换。

Developmental Switch of the Serotonergic Role in the Induction of Synaptic Long-term Potentiation in the Rat Visual Cortex.

机构信息

Department of Physiology, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea.

出版信息

Korean J Physiol Pharmacol. 2012 Feb;16(1):65-70. doi: 10.4196/kjpp.2012.16.1.65. Epub 2012 Feb 28.

Abstract

Synaptic long-term potentiation (LTP) and long-term depression (LTD) have been studied as mechanisms of ocular dominance plasticity in the rat visual cortex. Serotonin (5-hydroxytryptamine, 5-HT) inhibits the induction of LTP and LTD during the critical period of the rat visual cortex (postnatal 3~5 weeks). However, in adult rats, the increase in 5-HT level in the brain by the administration of the selective serotonin reuptake inhibitor (SSRI) fluoxetine reinstates ocular dominance plasticity and LTP in the visual cortex. Here, we investigated the effect of 5-HT on the induction of LTP in the visual cortex obtained from 3- to 10-week-old rats. Field potentials in layer 2/3, evoked by the stimulation of underlying layer 4, was potentiated by theta-burst stimulation (TBS) in 3- and 5-week-old rats, then declined to the baseline level with aging to 10 weeks. Whereas 5-HT inhibited the induction of LTP in 5-week-old rats, it reinstated the induction of N-methyl-D-aspartate receptor (NMDA)-dependent LTP in 8- and 10-week-old rats. Moreover, the selective SSRI citalopram reinstated LTP. The potentiating effect of 5-HT at 8 weeks of age was mediated by the activation of 5-HT(2) receptors, but not by the activation of either 5-HT(1A) or 5-HT(3) receptors. These results suggested that the effect of 5-HT on the induction of LTP switches from inhibitory in young rats to facilitatory in adult rats.

摘要

突触长时程增强(LTP)和长时程抑制(LTD)已被研究为大鼠视觉皮层眼优势可塑性的机制。5-羟色胺(5-HT)抑制大鼠视觉皮层关键期(出生后 3~5 周)LTP 和 LTD 的诱导。然而,在成年大鼠中,选择性 5-羟色胺再摄取抑制剂(SSRI)氟西汀增加脑内 5-HT 水平可恢复视觉皮层的眼优势可塑性和 LTP。在这里,我们研究了 5-HT 对 3-10 周龄大鼠视觉皮层 LTP 诱导的影响。用层 4 下刺激诱发的层 2/3 场电位,在 3 和 5 周龄大鼠中经 theta 爆发刺激(TBS)增强,然后随年龄增长至 10 周降至基线水平。虽然 5-HT 抑制了 5 周龄大鼠 LTP 的诱导,但它恢复了 8 周龄和 10 周龄大鼠 NMDA 受体(NMDA)依赖性 LTP 的诱导。此外,选择性 SSRI 西酞普兰也恢复了 LTP。8 周龄时 5-HT 的增强作用是通过激活 5-HT2 受体介导的,但不是通过激活 5-HT1A 或 5-HT3 受体介导的。这些结果表明,5-HT 对 LTP 诱导的作用在幼鼠中从抑制作用转变为成年鼠中的促进作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a080/3298828/557c27e4bf86/kjpp-16-65-g001.jpg

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