Distribution of AP-2 subtypes in the adult mouse brain

Citation
M. Shimada et al., Distribution of AP-2 subtypes in the adult mouse brain, NEUROSCI RE, 33(4), 1999, pp. 275-280
Citations number
19
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROSCIENCE RESEARCH
ISSN journal
01680102 → ACNP
Volume
33
Issue
4
Year of publication
1999
Pages
275 - 280
Database
ISI
SICI code
0168-0102(199904)33:4<275:DOASIT>2.0.ZU;2-W
Abstract
In the mammalian central nervous system (CNS), transcription factor activat or protein 2 (AP-2) is one of the critical regulatory factors for neural ge ne expression and neural development. As AP-2 has diverged into several sub types, i.e. AP-2 alpha, -2 beta, and 2.2, we investigated the distribution of the AP-2 subtypes in the adult mouse brain by in situ hybridization usin g subtype-specific probes. Though AP-2 was essentially expressed in most re gions of the brain, the hippocampus and cerebellum Purkinje cells exhibited a relatively high concentration of transcripts of any of the AP-2 subtypes . Among AP-2 alpha variants, the expression of Variant 1 was considerably l ower than that of variant 3. Hence, the expression pattern of AP-2 alpha va riant 3 is suggested to represent the major gene expression of AP-2 alpha. On the other hand, the expression of AP-2 beta messenger RNA (mRNA) was hig her than that of AP-2 alpha in many regions. Especially, the olfactory bulb , hippocampus, cerebellum, and cerebral cortex contained an abundance of th ese mRNAs. Different from those of AP-2 alpha, AP-2 beta mRNAs were detecte d in considerable amounts in the glanular cells as well as in Purkinje cell s. AP-2.2 gene expression was weak throughout the brain. Consequently, we f ound that various AP-2 subtypes and variants were expressed in a similar di stribution pattern with each having its own specific intensity but that the ir precise distribution profiles were not exactly the same. In the mature b rain, AP-2 is thought to regulate neural gene expression through specific a nd redundant association with a target gene. (C) 1999 Elsevier Science Irel and Ltd. All rights reserved.