Distribution and development of P2Y1-purinoceptors in the mouse retina

Rai, Dilip; Ishii, Takeaki; Imada, Hajime; Wada‐Kiyama, Yuko; Kiyama, Ryoiti; Miyachi, Ei-ichi; Kaneda, Makoto

doi:10.1007/s10735-013-9525-4

Cited by 11 publications

(8 citation statements)

References 37 publications

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“…In mice, deletion of P2Y 1 (which are expressed by Müller cells and populations of inner retinal neurons such as retinal ganglion cells and cholinergic amacrines; Ward and Fletcher, 2009;Wurm et al, 2010;Dilip et al, 2013) is associated with an increased survival of amacrine cells after retinal ischemiaereperfusion while the ischemic death of photoreceptor cells is more pronounced . These data suggest that P2Y 1 signaling (likely in glial cells) supports the survival of photoreceptors, and that P2Y 1 signaling in amacrines (Ward and Fletcher, 2009;Dilip et al, 2013) is involved in mediating the degeneration of the cells in the ischemic retina , likely by increasing cytotoxic calcium signaling. In the zebrafish retina, P2Y 1 activation by endogenous ADP has a protective role for inner retinal neurons after cytotoxic injury (Battista et al, 2009).…”

Section: Purinergic Regulation Of Retinal Cell Deathmentioning

confidence: 99%

Purinergic signaling in retinal degeneration and regeneration

Reichenbach

Bringmann

2016

Neuropharmacology

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Section: Purinergic Regulation Of Retinal Cell Deathmentioning

confidence: 99%

Purinergic signaling in retinal degeneration and regeneration

Reichenbach

Bringmann

2016

Neuropharmacology

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“…P2Y 1,2,4,6 18 21 22 23 24 25 and P2Y 11 (Zhang and Zhong, unpublished data) are expressed in rat GCs. There are two P2Y antagonists now commercially available, MRS2500, a selective P2Y 1 antagonist 47 and NF157, a selective P2Y 11 antagonist 48 .…”

Section: Resultsmentioning

confidence: 99%

“…Expression of P2 receptors has been described in rat retinal neurons and Müller cells 17 18 19 20 21 22 23 24 25 . In the retina, ATP released by Müller cells may act on both neurons and Müller cells 15 16 .…”

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confidence: 99%

Signaling mechanism for modulation by ATP of glycine receptors on rat retinal ganglion cells

Zhang

Zhou

et al. 2016

Sci Rep

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ATP modulates voltage- and ligand-gated channels in the CNS via the activation of ionotropic P2X and metabotropic P2Y receptors. While P2Y receptors are expressed in retinal neurons, the function of these receptors in the retina is largely unknown. Using whole-cell patch-clamp techniques in rat retinal slice preparations, we demonstrated that ATP suppressed glycine receptor-mediated currents of OFF type ganglion cells (OFF-GCs) dose-dependently, and the effect was in part mediated by P2Y1 and P2Y11, but not by P2X. The ATP effect was abolished by intracellular dialysis of a Gq/11 protein inhibitor and phosphatidylinositol (PI)-phospholipase C (PLC) inhibitor, but not phosphatidylcholine (PC)-PLC inhibitor. The ATP effect was accompanied by an increase in [Ca2+]i through the IP3-sensitive pathway and was blocked by intracellular Ca2+-free solution. Furthermore, the ATP effect was eliminated in the presence of PKC inhibitors. Neither PKA nor PKG system was involved. These results suggest that the ATP-induced suppression may be mediated by a distinct Gq/11/PI-PLC/IP3/Ca2+/PKC signaling pathway, following the activation of P2Y1,11 and other P2Y subtypes. Consistently, ATP suppressed glycine receptor-mediated light-evoked inhibitory postsynaptic currents of OFF-GCs. These results suggest that ATP may modify the ON-to-OFF crossover inhibition, thus changing action potential patterns of OFF-GCs.

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“…CAs express several P2 purinoceptors (Dilip et al 2013;Kaneda et al 2004Kaneda et al , 2008Shigematsu et al 2007;Ward et al 2008), and therefore the actions of ATP are not solely mediated by P2X 2 purinoceptors. To confirm the choline permeability to P2 purinoceptors and to identify the responsible P2 purinoceptors, we conducted electrophysiological recordings from dissociated retinal preparations in which anatomical information of the soma was lost; accordingly, GFP-positive cells responsive to ATP, which consist predominantly of OFF-CAs, were used for analysis (Fig.…”

Section: Resultsmentioning

confidence: 99%

Novel channel-mediated choline transport in cholinergic neurons of the mouse retina

Ishii

Homma

Mano

et al. 2017

Journal of Neurophysiology

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Choline uptake into the presynaptic terminal of cholinergic neurons is mediated by the high-affinity choline transporter and is essential for acetylcholine synthesis. In a previous study, we reported that P2X purinoceptors are selectively expressed in OFF-cholinergic amacrine cells of the mouse retina. Under specific conditions, P2X purinoceptors acquire permeability to large cations, such as -methyl-d-glucamine, and therefore potentially could act as a noncanonical pathway for choline entry into neurons. We tested this hypothesis in OFF-cholinergic amacrine cells of the mouse retina. ATP-induced choline currents were observed in OFF-cholinergic amacrine cells, but not in ON-cholinergic amacrine cells, in mouse retinal slice preparations. High-affinity choline transporters are expressed at higher levels in ON-cholinergic amacrine cells than in OFF-cholinergic amacrine cells. In dissociated preparations of cholinergic amacrine cells, ATP-activated cation currents arose from permeation of extracellular choline. We also examined the pharmacological properties of choline currents. Pharmacologically, α,β-methylene ATP did not produce a cation current, whereas ATPγS and benzoyl-benzoyl-ATP (BzATP) activated choline currents. However, the amplitude of the choline current activated by BzATP was very small. The choline current activated by ATP was strongly inhibited by pyridoxalphosphate-6-azophenyl-2',4'-sulfonic acid. Accordingly, P2X purinoceptors expressed in HEK-293T cells were permeable to choline and similarly functioned as a choline uptake pathway. Our physiological and pharmacological findings support the hypothesis that P2 purinoceptors, including P2X purinoceptors, function as a novel choline transport pathway and may provide a new regulatory mechanism for cholinergic signaling transmission at synapses in OFF-cholinergic amacrine cells of the mouse retina. Choline transport across the membrane is exerted by both the high-affinity and low-affinity choline transporters. We found that choline can permeate P2 purinergic receptors, including P2X purinoceptors, in cholinergic neurons of the retina. Our findings show the presence of a novel choline transport pathway in cholinergic neurons. Our findings also indicate that the permeability of P2X purinergic receptors to choline observed in the heterologous expression system may have a physiological relevance in vivo.

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Distribution and development of P2Y1-purinoceptors in the mouse retina

Cited by 11 publications

References 37 publications

Purinergic signaling in retinal degeneration and regeneration

Purinergic signaling in retinal degeneration and regeneration

Signaling mechanism for modulation by ATP of glycine receptors on rat retinal ganglion cells

Novel channel-mediated choline transport in cholinergic neurons of the mouse retina

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