Satoko Hamada

GPR155: Gene organization, multiple mRNA splice variants and expression in mouse central nervous system

Emerging evidence suggests that GPR155, an integral membrane protein related to G-protein coupled receptors, has specific roles in Huntington disease and autism spectrum disorders. This study reports the structural organization of mouse GPR155 gene and the generation of five variants (Variants 1-5) of GPR155 mRNA, including so far unknown four variants. Further, it presents the level of expression of GPR155 mRNA in different mouse tissues. The mRNAs for GPR155 are widely expressed in adult mouse tissues and during development. In situ hybridization was used to determine the distribution of GPR155 in mouse brain. The GPR155 mRNAs are widely distributed in forebrain regions and have more restricted distribution in the midbrain and hindbrain regions. The highest level of expression was in the lateral part of striatum and hippocampus. The expression pattern of GPR155 mRNAs in mouse striatum was very similar to that of cannabinoid receptor type 1. The predicted protein secondary structure indicated that GPR155 is a 17-TM protein, and Variant 1 and Variant 5 proteins have an intracellular, conserved DEP domain near the C-terminal.

Histological Determination of the Areas Enriched in Cholinergic Terminals and m2 and m3 Muscarinic Receptors in the Mouse Central Auditory System

Cholinergic projections to auditory system are vital for coupling arousal with sound processing. Systematic search with in situ hybridization and immunohistochemistry indicated that the ventral nucleus of the medial geniculate body and the nucleus of the brachium of the inferior colliculus constituted cholinergic synaptic sites in the brainstem auditory system, containing a significant number of cholinergic axon terminals and m2 receptor‐expressing cell bodies. Anat Rec 293:1393–1399, 2010.

Increase in GAD2 expression in the periolivary region of the mouse following cochlear ablation

O2P-BØ3 Strength of GABAergic transmission influences climbing fiber synapse elimination during cerebellar development Hisako Nakayama1, Kouichi Hashimoto1,2, Taisuke Miyazaki3, Yuchio Yanagawa4, Kunihiko Obata5, Masahiko Watanabe3, Masanobu Kano1 1 Graduate School of Medicine, Osaka University, Osaka, Japan; 2 CREST-JST, Kawaguchi, Japan; 3 Graduate School of Medicine, Hokkaido University, Sapporo, Japan; 4 Graduate School of Medicine, Gunma University, Maebashi, Japan; 5 RIKEN, BSI, Wako, Japan