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嗅觉视网膜离心输入调节斑马鱼视网膜神经节细胞的活动:多巴胺介导的Ca2+信号通路的可能作用。

Olfactoretinal centrifugal input modulates zebrafish retinal ganglion cell activity: a possible role for dopamine-mediated Ca2+ signalling pathways.

作者信息

Huang Luoxiu, Maaswinkel Hans, Li Lei

机构信息

Department of Biological Sciences, University of Notre Dame, Notre Dame, IN 46556, USA.

出版信息

J Physiol. 2005 Dec 15;569(Pt 3):939-48. doi: 10.1113/jphysiol.2005.099531. Epub 2005 Oct 20.

Abstract

The vertebrate retina receives centrifugal input from the brain. In zebrafish, the major centrifugal input originates in the terminal nerve (TN). TN cell bodies are located in the olfactory bulb and ventral telencephalon. The TN projects axons to the retina where they branch in the inner plexiform layer (IPL) and synapse onto several inner retinal cell types, including dopaminergic interplexiform cells (DA-IPCs). This olfactoretinal centrifugal input plays a role in modulating retinal ganglion cell (RGC) activity, probably via dopamine-mediated Ca2+ signalling pathways. Normally, dopamine inhibits RGC firing by decreasing the inward Ca2+ current. Olfactory stimulation with amino acids decreases dopamine release in the retina, thereby reducing dopaminergic inhibition of RGCs. This model of olfacto-visual integration was directly tested by recording single-unit RGC activity in response to olfactory stimulation in the presence or absence of dopamine receptor blockers. Stimulation of the olfactory neurones increased RGC activity. However, this effect diminished when the dopamine D1 receptors were pharmacologically blocked. In isolated RGCs, the application of dopamine or a dopamine D1 receptor agonist decreased voltage-activated Ca2+ current and lowered Ca2+ influx. Together, the data suggest that olfactory input has a modulatory effect on RGC firing, and that this effect is mediated by dopamine D1 receptor-coupled Ca2+ signalling pathways.

摘要

脊椎动物的视网膜接收来自大脑的离心输入。在斑马鱼中,主要的离心输入起源于终末神经(TN)。TN细胞体位于嗅球和腹侧端脑。TN将轴突投射到视网膜,在那里它们在内网状层(IPL)分支并与几种视网膜内层细胞类型形成突触,包括多巴胺能网间细胞(DA-IPC)。这种嗅觉-视网膜离心输入可能通过多巴胺介导的Ca2+信号通路在调节视网膜神经节细胞(RGC)活动中发挥作用。正常情况下,多巴胺通过减少内向Ca2+电流来抑制RGC放电。用氨基酸进行嗅觉刺激会减少视网膜中的多巴胺释放,从而降低多巴胺能对RGC的抑制作用。通过记录在存在或不存在多巴胺受体阻滞剂的情况下对嗅觉刺激作出反应的单单位RGC活动,直接测试了这种嗅觉-视觉整合模型。刺激嗅觉神经元会增加RGC活动。然而,当多巴胺D1受体被药理阻断时,这种效应会减弱。在分离的RGC中,应用多巴胺或多巴胺D1受体激动剂会降低电压激活的Ca2+电流并减少Ca2+内流。总之,数据表明嗅觉输入对RGC放电有调节作用,并且这种作用是由多巴胺D1受体偶联的Ca2+信号通路介导的。

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