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多巴胺选择性增强海马苔藓纤维至CA3突触传递。

Dopamine selectively potentiates hippocampal mossy fiber to CA3 synaptic transmission.

作者信息

Kobayashi Katsunori, Suzuki Hidenori

机构信息

Department of Pharmacology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8602, Japan.

出版信息

Neuropharmacology. 2007 Feb;52(2):552-61. doi: 10.1016/j.neuropharm.2006.08.026. Epub 2006 Oct 13.

Abstract

Dopamine has been implicated in various brain functions and the pathology of neurological diseases. In the hippocampus, dopamine has been shown to induce acute depression of synaptic transmission in the CA1 region, but it remains largely unknown how it works in the CA3 region. We here report that dopamine induces acute synaptic potentiation at the synapse formed by mossy fibers (MFs) on mouse hippocampal CA3 pyramidal cells, but not at converging associational/commissural synapses. Dopamine potentiated both alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and N-methyl-d-aspartate (NMDA) components of MF synaptic responses similarly in respect of the magnitude and time course. The dopamine-induced potentiation was intact in the presence of picrotoxin, required activation of D(1)-like receptors and was apparently occluded by an activator of adenylate cyclase. The potentiation was accompanied by a decrease in magnitude of synaptic facilitation, suggesting the presynaptic site for the expression of the potentiation. The present study is the first demonstration of acute potentiation of hippocampal excitatory synaptic transmission by dopamine, which is most probably mediated by presynaptic D(1)-like receptor-cAMP cascades.

摘要

多巴胺与多种脑功能以及神经疾病的病理过程有关。在海马体中,多巴胺已被证明可诱导CA1区突触传递的急性抑制,但它在CA3区如何发挥作用在很大程度上仍不清楚。我们在此报告,多巴胺可诱导苔藓纤维(MFs)与小鼠海马CA3锥体细胞形成的突触处出现急性突触增强,但在汇聚的联合/连合突触处则不会。多巴胺对MF突触反应的α-氨基-3-羟基-5-甲基-4-异恶唑丙酸(AMPA)和N-甲基-D-天冬氨酸(NMDA)成分的增强作用在幅度和时间进程方面相似。在存在荷包牡丹碱的情况下,多巴胺诱导的增强作用仍然存在,需要激活D(1)样受体,并且明显被腺苷酸环化酶激活剂所阻断。这种增强作用伴随着突触易化幅度的降低,表明增强作用的表达位于突触前部位。本研究首次证明了多巴胺对海马兴奋性突触传递的急性增强作用,这很可能是由突触前D(1)样受体-cAMP级联反应介导的。

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