Regional distribution of regulators of G-protein signaling (RGS) 1, 2, 13,14, 16, and GAIP messenger ribonucleic acids by in situ hybridization in rat brain
E. Grafstein-dunn et al., Regional distribution of regulators of G-protein signaling (RGS) 1, 2, 13,14, 16, and GAIP messenger ribonucleic acids by in situ hybridization in rat brain, MOL BRAIN R, 88(1-2), 2001, pp. 113-123
Regulators of G-protein signaling (RGS) proteins are a novel family of GTPa
se-activating proteins that interact with Ga subunits of the Gi/o, Gz, Gq a
nd G(12/13) subfamilies to dampen G-protein-coupled receptor (GPCR)-mediate
d signaling by accelerating intrinsic G alpha -GTPase activity. In the pres
ent study, we report on messenger ribonucleic acid (mRNA) localization in r
at brain of six RGS genes by in situ hybridization. The distribution patter
ns of RGS2, RGS13, RGS14 and GAIP (Ga interacting protein) overlapped in mo
st brain regions examined. Highest regional expression was observed for RGS
2 in the cerebral cortical layers: striatum, hippocampal formation, several
thalamic and hypothalamic nuclei and hindbrain regions such as the pontine
, interpeduncular and dorsal raphe nuclei. Levels of RGS14 mRNA closely par
alleled those of RGS2 expression levels throughout most brain regions. RGS1
3 mRNA was enriched in the hippocampal formation, amygdala, mammillary nucl
ei as well as the pontine and interpeduncular nuclei. GAIP expression level
s were highest in the hippocampal formation with moderate to low levels pre
sent in all other regions studied. Of the six RGS genes probed, RGS 16 mRNA
displayed a discrete localization predominantly in the thalamic midline/in
tralaminar and principal relay nuclei, and the hypothalamic suprachiasmatic
nucleus. RGS1 mRNA signal was not detected in brain. In conclusion, the in
situ hybridization studies for RGS2, RGS13, RGS14, RGS16 and GAIP mRNAs ex
tend our knowledge of the distribution of RGS genes expressed in the rat ce
ntral nervous system, and indicate overlapping RGS-enriched regions that ma
y be indicative of functional diversification in GPCR signaling pathway mod
ulation. (C) 2001 Elsevier Science B.V. All rights reserved.