RT Journal Article
SR Electronic
T1 Differential expression of AMPA receptor subunits in NOS-positive neurons of cortex, striatum, and hippocampus
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 7046
OP 7061
DO 10.1523/JNEUROSCI.15-11-07046.1995
VO 15
IS 11
A1 Catania, MV
A1 Tolle, TR
A1 Monyer, H
YR 1995
UL http://www.jneurosci.org/content/15/11/7046.abstract
AB AMPA receptor (AMPAR) subunits expression was studied in nitric oxide synthase (NOS)-positive neurons of the adult rat cortex, striatum, and hippocampus, by a double-labeling approach, combining nonradioactive in situ hybridization and immunocytochemistry. The majority of cortical and hippocampal NOS-immunopositive neurons were characterized by a predominant expression of GluR-A and -D mRNA and low or undetectable expression of GluR-B and -C mRNA. In the striatum, the expression profile of AMPAR subunits in NOS-positive neurons differed from that in the other two regions. This is reflected in the overall low expression of all AMPA receptor subunits and the paucity of GluR-D subunit expression that contrasts with the high expression of this subunit in NOS-positive cells in the hippocampus. Double-labeling experiments revealed a substantial correspondence between mRNA and protein levels of AMPAR subunits. Further evidence for the regional diversity of NOS- positive neurons is derived from the expression analysis of glutamate decarboxylase (GAD)-65 and -67 mRNAs. NOS-positive neurons expressed high levels of GAD-65, but not -67 in the cortex, high levels of both forms in the hippocampus, and low or undetectable levels of both mRNAs in the striatum. Despite of these differences, NOS-positive neurons share the common feature of low GluR-B subunit expression, suggesting the presence of AMPAR channels with high Ca2+ permeability, regardless of the regional location. The relative resistance of NOS-positive interneurons in neurodegenerative diseases suggests that glutamate receptor-mediated Ca2+ influx alone does not suffice to explain neuronal vulnerability, and additional factors have thus to be considered.