Properties and functions of TRPM1 channels in the dendritic tips of retinal ON-bipolar cells

被引:25
作者
Schneider, Franziska M. [1 ]
Mohr, Florian [1 ]
Behrendt, Marc [1 ]
Oberwinkler, Johannes [1 ]
机构
[1] Univ Marburg, Inst Physiol & Pathophysiol, D-35037 Marburg, Germany
关键词
TRPM1; Retina; ON-bipolar cells; Synapse; Congenital stationary night blindness (CSNB); G-protein-coupled signaling; STATIONARY NIGHT BLINDNESS; METABOTROPIC GLUTAMATE-RECEPTOR; RICH REPEAT PROTEIN; MELANOMA-ASSOCIATED RETINOPATHY; POTENTIAL CATION CHANNEL; PANCREATIC BETA-CELLS; LIGHT RESPONSE; ROD BIPOLAR; SIGNALING COMPLEX; MAMMALIAN RETINA;
D O I
10.1016/j.ejcb.2015.06.005
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
An increase in light intensity induces a depolarization in retinal ON-bipolar cells via a reduced glutamate release from presynaptic photoreceptor cells. The underlying transduction cascade in the dendritic tips of ON-bipolar cells involves mGluR6 glutamate receptors signaling to TRPM1 proteins that are an indispensable part of the transduction channel. Several other proteins are recognized to participate in the transduction machinery. Deficiency in many of these leads to congenital stationary night blindness, because rod bipolar cells, a subgroup of ON-bipolar cells, constitute the main route for sensory information under scotopic conditions. Here, we review the current knowledge about TRPM1 ion channels and how their activity is regulated within the postsynaptic compartment of ON-bipolar cells. The functional properties of TRPM1 channels in the dendritic compartment are not well understood as they differ substantially from those of recombinant TRPM1 channels. Critical evaluation of possible explanations of these discrepancies indicates that some key components of this transduction pathway might still not be known. The continued exploration of this pathway will yield further clinically useful insights. (C) 2015 Elsevier GmbH. All rights reserved.
引用
收藏
页码:420 / 427
页数:8
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