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GABA A and GABA C receptors on mammalian rod bipolar cells
Author(s) -
Fletcher Erica L.,
Koulen Peter,
Wässle Heinz
Publication year - 1998
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/(sici)1096-9861(19980706)396:3<351::aid-cne6>3.0.co;2-1
Subject(s) - gabaa receptor , gabaa rho receptor , inner plexiform layer , receptor , microbiology and biotechnology , biology , gabaergic , synapse , protein subunit , retina , neuroscience , chemistry , biochemistry , gene
Rod bipolar (RB) cells of mammalian retinae receive synapses from different γ‐aminobutyric acid (GABAergic) amacrine cells in the inner plexiform layer (IPL). We addressed the question whether RB cells of the rabbit and of the rat retina express different types of GABA receptors at these synapses. RB cells were immunolabeled in vertical sections of rat retinae with an antibody against protein kinase C (PKC). The sections were double‐labled for the α1, α2, α3, or γ2 subunits of the GABA A receptor. Punctate immunofluorescence, which represents synaptic localization, was found for all four subunits. Many of the α1‐, α3‐, or γ2‐immunoreactive puncta coincided with the axon terminals of the PKC‐immunolabeled RB cells. Sections and wholemounts of rabbit retinae were also double labeled for PKC and the ρ subunits of the GABA C receptor. Rabbit RB cells were decorated by many ρ‐immunoreactive puncta, which were shown by electron microscopy to represent synaptic localization. Previous work from our laboratory has shown that the α1, α2, α3, and ρ subunits are not found within the same synapse but are expressed at different synaptic sites. Taken together, these results suggest that RB cells of mammalian retinae express at least three different types of GABA receptors at synaptic sites in the IPL: GABA C receptors, GABA A receptors containing the α1 subunit, and GABA A receptors containing the α3 subunit. J. Comp. Neurol. 396:351–365, 1998. © 1998 Wiley‐Liss, Inc.