Neurogranin is expressed by principal cells but not interneurons in the rodent and monkey neocortex and hippocampus
Version of Record online: 23 SEP 2004
Copyright © 2004 Wiley-Liss, Inc.
Journal of Comparative Neurology
Volume 479, Issue 1, pages 30–42, 1 November 2004
How to Cite
Singec, I., Knoth, R., Ditter, M., Volk, B. and Frotscher, M. (2004), Neurogranin is expressed by principal cells but not interneurons in the rodent and monkey neocortex and hippocampus. J. Comp. Neurol., 479: 30–42. doi: 10.1002/cne.20302
- Issue online: 23 SEP 2004
- Version of Record online: 23 SEP 2004
- Manuscript Accepted: 2 JUL 2004
- Manuscript Revised: 21 MAY 2004
- Manuscript Received: 28 APR 2003
- Deutsche Forschungsgemeinschaft. Grant Numbers: SFB 505, SFB TR-3
- protein kinase C;
- calcium signaling
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.  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.