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Quantitative gene‐expression analysis of the ligand‐receptor system for classical neurotransmitters and neuropeptides in hippocampal CA1, CA3, and dentate gyrus
Author(s) -
Nakamura Nozomu H.,
Akiyama Kiyotaka,
Naito Takayuki
Publication year - 2011
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.20830
Subject(s) - ionotropic effect , dentate gyrus , hippocampal formation , neuropeptide , receptor , neuroscience , ionotropic glutamate receptor , receptor expression , glutamate receptor , biology , chemistry , biochemistry
We have shown quantitative expression levels of genes coding for the “ligand‐receptor system” for classical neurotransmitters and neuropeptides in hippocampal subregions CA1, CA3, and dentate gyrus (DG). Using a combination of DNA microarray and quantitative PCR methods, we found that the three subregions have relatively similar expression patterns of ionotropic receptors for classical neurotransmitters. Expression of ionotropic receptors for glutamate and GABA represents more than 90% of all ionotropic receptors for classical neurotransmitters, and the expression ratio between ionotropic receptors for glutamate and GABA is constant (1.2:1–1.6:1) in each subregion. Meanwhile, the three subregions have different expression patterns of neuropeptide receptors. Furthermore, there are asymmetric expression patterns between neuropeptides and their receptors. Expression of Cck , Npy , Sst , and Penk1 represents 90% of neuropeptides derived locally in the hippocampus, whereas expression of these four neuropeptide receptors accounts for 50% of G protein‐coupled receptors for neuropeptides. We propose that CA1, CA3, and DG have different modalities based on the ligand‐receptor system, particularly the “neuropeptidergic system.” Our quantitative gene‐expression analysis provides fundamental data to support functional differences between the three hippocampal subregions regarding ligand‐receptor interactions. © 2010 Wiley Periodicals, Inc.