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Neurogranin is expressed by principal cells but not interneurons in the rodent and monkey neocortex and hippocampus
Author(s) -
Singec Ilyas,
Knoth Rolf,
Ditter Margarethe,
Volk Benedikt,
Frotscher Michael
Publication year - 2004
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.20302
Subject(s) - biology , calretinin , parvalbumin , neuroscience , neocortex , hippocampal formation , neurogranin , dentate gyrus , hippocampus , cerebellum , gabaergic , population , excitatory postsynaptic potential , interneuron , synaptic plasticity , inhibitory postsynaptic potential , microbiology and biotechnology , protein kinase c , signal transduction , biochemistry , immunology , receptor , immunohistochemistry , demography , sociology
As a substrate of protein kinase C (PKC), neurogranin (NG) is involved in the regulation of calcium signaling and activity‐dependent plasticity. Recently, we have shown that, in the rodent cerebellum, NG is exclusively expressed by γ‐aminobutyric acidergic Golgi cells, whereas, in the monkey cerebellum, brush cells were the only neuronal population expressing NG (Singec et al. [2003] J. Comp. Neurol. 459:278–289). In the present study, we analyzed the neocortical and hippocampal expression patterns of NG in adult mouse (C57Bl/6), rat (Wistar), and monkey ( Cercopithecus aetiops ). By using immunocytochemistry and nonradioactive in situ hybridization, we demonstrate strong NG expression by principal cells in different neocortical layers and in the hippocampus by granule cells of the dentate gyrus and pyramidal neurons of CA1–CA3. In contrast, double‐labeling experiments in rodents revealed that neocortical and hippocampal interneurons expressing glutamate decarboxylase 67 (GAD67) were consistently devoid of NG. In addition, by using antibodies against parvalbumin, calbindin, and calretinin, we could demonstrate the absence of NG in interneurons of monkey frontal cortex and hippocampus. Together these findings corroborate the idea of different calcium signaling pathways in excitatory and inhibitory cells that may contribute to different modes of synaptic plasticity in these neurons. J. Comp. Neurol. 479:30–42, 2004. © 2004 Wiley‐Liss, Inc.