Behavioral testing upregulates pCaMKII, BDNF, PSD-95 and egr-1 in hippocampus of FVB/N mice.
Several protein cascades are proposed to be involved in the formation of synaptic plasticity and have been linked to neuronal information processing and storage. Although modified expression of specific proteins following behavioral testing has been shown, no systematic approach for their concomitant determination has been reported. We therefore determined hippocampal expression of signaling proteins, transcription factors and synaptosomal-associated proteins representing key elements of neuronal plasticity in mice following behavioral training. Male FVB/N mice, 12 weeks of age, were used for behavioral testing. After completion of tests mice were sacrificed and hippocampi were dissected. Levels of total and autophosphorylated (T286) alphacalcium-calmodulin dependent kinase II (CaMKII, pCaMKII), total and phosphorylated mitogen-activated protein kinase (MAPK, pMAPK), total and phosphorylated calcium-responsive element binding (creb, pcreb), early-growth response protein 1 (egr-1), brain derived neurotrophic factor (BDNF), tyrosine kinase receptor B (trk B), drebrin and postsynaptic density-95 (PSD-95) were quantified in hippocampi of behavior trained animals (n=7) and naïve caged controls (n=7). Expression of pCaMKII, BDNF, PSD-95 and egr-1 was significantly increased in the behavior-trained group. Expression of total CaMKII, total and pMAPK, total and pcreb, trk B and drebrin was comparable between groups. Detection of significantly increased pCaMKII, BDNF, PSD-95 and egr-1 induced by behavioral training at the protein level per se is intriguing and supports the proposed importance of these molecules for neuronal information storage.[1]References
- Behavioral testing upregulates pCaMKII, BDNF, PSD-95 and egr-1 in hippocampus of FVB/N mice. Pollak, D.D., Herkner, K., Hoeger, H., Lubec, G. Behav. Brain Res. (2005) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg









