Expression of glycine receptor and transporter on bullfrog retinal Müller cells

Lee, Shu-Chen; Zhong, Yong-Mei; Yang, Xiong‐Li

doi:10.1016/j.neulet.2005.06.023

Cited by 24 publications

(28 citation statements)

References 24 publications

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“…Our immunocytochemical study confirmed previous reports that GlyT-1 is expressed in amacrine cells in the inner nuclear and inner plexifom layers and also in Müller glia cells of rat retina [6,68]. In OGD-induced neurotoxicity, glycine may be released by reverse mode operation of GlyT-1 from Müller glia cells and by spillover from synapses of glycinergic amacrine cells: mechanisms that have roles to build up extrasynaptic glycine levels [31].…”

Section: Possible Pathological Implications: Therapeutic Interventionsupporting

confidence: 91%

“…In vertical section of rat retina, GFAP immunofluoresence was found in the nerve fiber layer, inner nuclear layer and the inner and outer plexiform layers. Thus, the appearance of GlyT-1 immunoreactivity confirms previous findings demonstrating expression of GlyT-1 in glycinergic amacrine cells and Müller glia cells, respectively [4,6]. …”

Section: Immunocytochemical Staining Of Glyt-1 In Retinal Cellssupporting

confidence: 90%

“…Müller cells, including the somata in the nerve fiber layer á (thin arrow), the major processes in the IPL and OPL, and the endfeet in the nerve fiber layer (arrowhead), are visible with appearance of GFAP immunoreactivity. The GFAP immunoreactive Müller cells also showed immunostaining for GlyT-1 confirming previous findings of Lee et al [6]. In addition, expression of GlyT-1 was visible in glycinergic amacrine cells in the INL (thick arrow) and their dendrites descending into IPL [4,9].…”

Section: Oxygen-glucose Deprivation and [ 3 H]glycine Release In Rat supporting

confidence: 89%

“…Glycine is released from retinal amacrine cells and Müller glial cells and its synaptic and extrasynaptic concentrations are regulated by glycine transporter type-1 (GlyT-1) [3][4][5][6]. In physiological conditions, the GlyT-1 mediated uptake prevents accumulation of glycine extracellularly and thus minimizes the possibility of glycine/glutamate neurotoxicity triggered by overstimulation of NMDA receptors.…”

Section: Introductionmentioning

confidence: 99%

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Some Operational Characteristics of Glycine Release in Rat Retina: The Role of Reverse Mode Operation of Glycine Transporter Type-1 (GlyT-1) in Ischemic Conditions

et al. 2015

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Rat posterior eyecups containing the retina were prepared, loaded with [(3)H]glycine and superfused in order to determine its release originated from glycinergic amacrine cells and/or glial cells. Deprivation of oxygen and glucose from the Krebs-bicarbonate buffer used for superfusion evoked a marked increase of [(3)H]glycine release, an effect that was found to be external Ca(2+)-independent. Whereas oxygen and glucose deprivation increased [(3)H]glycine release, its uptake was reduced suggesting that energy deficiency shifts glycine transporter type-1 operation from normal to reverse mode. The increased release of [(3)H]glycine evoked by oxygen and glucose deprivation was suspended by addition of the non-competitive glycine transporter type-1 inhibitor NFPS and the competitive inhibitor ACPPB further suggesting the involvement of this transporter in the mediation of [(3)H]glycine release. Oxygen and glucose deprivation also evoked [(3)H]glutamate release from rat retina and the concomitantly occurring release of the NMDA receptor agonist glutamate and the coagonist glycine makes NMDA receptor pathological overstimulation possible in hypoxic conditions. [(3)H]Glutamate release was suspended by addition of the excitatory amino acid transporter inhibitor TBOA. Sarcosine, a substrate inhibitor of glycine transporter type-1, also increased [(3)H]glycine release probably by heteroexchange shifting transporter operation into reverse mode. This effect of sarcosine was also external Ca(2+)-independent and could be suspended by NFPS. Energy deficiency in retina induced by ouabain, an inhibitor of the Na(+)-K(+)-dependent ATPase, and by rotenone, a mitochondrial complex I inhibitor added with the glycolytic inhibitor 2-deoxy-D-glucose, led to increase of retinal [(3)H]glycine efflux. These effects of ouabain and rotenone/2-deoxy-D-glucose could also be blocked by NFPS pointed to the preferential reverse mode operation of glycine transporter type-1 as a consequence of impaired cellular energy homeostasis. Immunohistochemical studies revealed that glycine transporter type-1, of which reverse mode operation assures [(3)H]glycine release, is expressed in amacrine cells in the inner nuclear and plexiform layers of the retina and also in Müller macroglia cells. We conclude that disruption of the balanced normal/reverse mode operation of glycine transporter type-1 is likely a significant factor contributing to neurotoxic processes of the retina. The possibility to inhibit glycine transporter type-1 mediated glycine efflux by drugs more potently than glycine uptake might offer some therapeutic potential for the treatment of various neurodegenerative disorders of the retina.

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Section: Possible Pathological Implications: Therapeutic Interventionsupporting

confidence: 91%

Section: Immunocytochemical Staining Of Glyt-1 In Retinal Cellssupporting

confidence: 90%

Section: Oxygen-glucose Deprivation and [ 3 H]glycine Release In Rat supporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Some Operational Characteristics of Glycine Release in Rat Retina: The Role of Reverse Mode Operation of Glycine Transporter Type-1 (GlyT-1) in Ischemic Conditions

et al. 2015

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“…22 They are also likely to be expressed by interneurons and could be expressed on glial cells. 23 Recent results showed high proliferation of oligodendrocyte precursor cells in tissue rostral and caudal to the epicenter. 24,25 Therefore, alteration in GlyRs could be due to damage to each of these sources of GlyR in the spinal cord.…”

Section: Discussionmentioning

confidence: 99%

Differential expression of glycine receptor subunit messenger RNA in the rat following spinal cord injury

Esmaeili

Zaker

2010

Spinal Cord

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Study design: Spinal cord injury (SCI) results in alterations in the regulation of many genes that may influence neuronal death and the subsequent loss of motor function and neuropathic pain. The subtype expression mRNA levels of glycine receptors (GlyRs) after SCI are unknown. Methods: Using real-time reverse transcription PCR, this study analyzed changes in the mRNA abundance of the four major GlyR subunits (a13 and b) at 6, 24 h and 3, 7 and 10 days after SCI in adult male rats. SCI was induced at the T9 level by transection. Results: Our results show a complicated temporal and spatial pattern of alteration in GlyR mRNA expression levels after SCI. Temporal and spatial variations with different degrees and direction (up or downregulation) of expression alteration were observed. The greatest variation was seen in GlyRa1, whereas GlyRa2 was downregulated in all regions following SCI. Conclusion: This study shows that alteration in GlyR expression starts as early as 6 h after SCI. The most significant points of this research are temporal elevation of GlyRa1 and continuous reduction of GlyRa2. Alterations in GlyR expression within the spinal cord may have a key role in the development of pathological pain. Therefore, control of GlyR expression could represent a novel therapeutic avenue for the development of new painkiller agents in SCI.

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Comparative electrophysiology of retinal Müller glial cells—A survey on vertebrate species

Pannicke

Chao²,

Reisenhofer

et al. 2016

Glia

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Müller cells are the dominant macroglial cells in the retina of all vertebrates. They fulfill a variety of functions important for retinal physiology, among them spatial buffering of K ions and uptake of glutamate and other neurotransmitters. To this end, Müller cells express inwardly rectifying K channels and electrogenic glutamate transporters. Moreover, a lot of voltage- and ligand-gated ion channels, aquaporin water channels, and electrogenic transporters are expressed in Müller cells, some of them in a species-specific manner. For example, voltage-dependent Na channels are found exclusively in some but not all mammalian species. Whereas a lot of data exist from amphibians and mammals, the results from other vertebrates are sparse. It is the aim of this review to present a survey on Müller cell electrophysiology covering all classes of vertebrates. The focus is on functional studies, mainly performed using the whole-cell patch-clamp technique. However, data about the expression of membrane channels and transporters from immunohistochemistry are also included. Possible functional roles of membrane channels and transporters are discussed. Obviously, electrophysiological properties involved in the main functions of Müller cells developed early in vertebrate evolution. GLIA 2017;65:533-568.

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Expression of glycine receptor and transporter on bullfrog retinal Müller cells

Cited by 24 publications

References 24 publications

Some Operational Characteristics of Glycine Release in Rat Retina: The Role of Reverse Mode Operation of Glycine Transporter Type-1 (GlyT-1) in Ischemic Conditions

Some Operational Characteristics of Glycine Release in Rat Retina: The Role of Reverse Mode Operation of Glycine Transporter Type-1 (GlyT-1) in Ischemic Conditions

Differential expression of glycine receptor subunit messenger RNA in the rat following spinal cord injury

Comparative electrophysiology of retinal Müller glial cells—A survey on vertebrate species

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