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RIM3γ is a postsynaptic protein in the rat central nervous system
Author(s) -
Liang Fengyi,
Zhang Bin,
Tang Junhong,
Guo Jing,
Li Wenbo,
Ling Eng Ang,
Chu Haiying,
Wu Yajun,
Chan Yee Gek,
Cao Qiong
Publication year - 2007
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.21403
Subject(s) - postsynaptic potential , biology , immunoelectron microscopy , postsynaptic density , microbiology and biotechnology , synaptophysin , synapse , neuroscience , neurotransmission , synaptic plasticity , in situ hybridization , messenger rna , immunohistochemistry , immunology , biochemistry , gene , receptor
RIMs (Rab3‐interacting molecules) are synaptic proteins essential for neural transmission and plasticity. RIM1α has been implicated in membrane trafficking and regulation of secretory vesicle exocytosis in eukaryotic cells. Little information is as yet available on RIM3γ. In the present study, we investigated the cellular expression, subcellular distribution, and possible functions of RIM3γ in the rat CNS. Rim3γ cDNA was subcloned and the protein expressed in vitro for the generation and purification of a rabbit anti‐RIM3γ polyclonal antibody. In situ hybridization histochemistry, immunohistochemistry, and immunoelectron microscopy were performed to map expression of the mRNA and protein in the rat CNS. Our results indicated widespread distribution of RIM3γ in diverse CNS neuronal cell types. The mRNA was found mainly in the cell bodies, whereas the protein immunoreactivity was localized chiefly to neuronal dendrites and to the postsynaptic densities as visualized under the light and electron microscope. This postsynaptic placement of RIM3γ is distinct from the presynaptic localization of RIM1α but may contribute to regulating synaptic transmission and plasticity. The identification of RIM3γ as a postsynaptic protein has functional implications for CNS synapse functions. J. Comp. Neurol. 503:501–510, 2007. © 2007 Wiley‐Liss, Inc.