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Diversity of glycine receptors in the mouse retina: Localization of the α2 subunit
Author(s) -
Haverkamp Silke,
Müller Ulrike,
Zeilhofer Hanns U.,
Harvey Robert J.,
Wässle Heinz
Publication year - 2004
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.20267
Subject(s) - glycine receptor , inner plexiform layer , gephyrin , amacrine cell , biology , glycine , retina , inhibitory postsynaptic potential , axon , postsynaptic potential , neuroscience , protein subunit , microbiology and biotechnology , receptor , biochemistry , amino acid , gene
Abstract γ‐Aminobutyric acid (GABA) and glycine are the major inhibitory neurotransmitters in the retina, glycine being produced in approximately half of all amacrine cells. Whereas retinal cell types expressing the glycine receptor (GlyR) α1 and α3 subunits have been mapped, the role of the α2 subunit in retinal circuitry remains unclear. By using immunocytochemistry, we localized the α2 subunit in the inner plexiform layer (IPL) in brightly fluorescent puncta, which represent postsynaptically clustered GlyRs. This was shown by doubly labeling sections for GlyR α2 and bassoon (a presynaptic marker) or gephyrin (a postsynaptic marker). Synapses containing GlyR α2 were rarely found on ganglion cell dendrites but were observed on bipolar cell axon terminals and on amacrine cell processes. Recently, an amacrine cell type has been described that is immunopositive for glycine and for the vesicular glutamate transporter vGluT3. The processes of this cell type were presynaptic to GlyR α2 puncta, suggesting that vGluT3 amacrine cells release glycine. Double labeling of sections for GlyR α1 and GlyR α2 subunits showed that they are clustered at different synapses. In sections doubly labeled for GlyR α2 and GlyR α3, approximately one‐third of the puncta were colocalized. The most abundant GlyR subtype in retina contains α3 subunits, followed by those containing GlyR α2 and GlyR α1 subunits. J. Comp. Neurol. 477:399–411, 2004. © 2004 Wiley‐Liss, Inc.