Strain-dependent regulation of plasticity-related proteins in the mouse hippocampus.

Inbred mouse strains have different genetic backgrounds that can result in impairment of synaptic plasticity and memory. Strain-dependent performance in behavioral and cognitive tasks is well-documented. Hippocampal long-term potentiation (LTP), an activity-dependent enhancement of synaptic transmission that may underlie some forms of learning and memory has been shown to differ significantly between inbred mouse strains. However, an effect of strain on the expression of proteins, critically involved in synaptic plasticity, learning and memory has not been described yet. We have been addressing this question by determining expressional levels of a panel of proteins involved in neuronal information processing in hippocampus of five mouse strains by immunoblotting. Four inbred strains (FVB/N, C57Bl/6J, 129S2/Sv and Balb/c), commonly used for generating genetically modified mice and for conventional experiments in pharmacology and toxicology and one outbred strain (OF1) have been selected. A significant effect of strain was detected for total and phosphorylated calcium-calmodulin dependent kinase IIalpha (CaMKII, pCaMKII), phosphorylated mitogen-activated protein kinase (pMAPK), total and phosphorylated calcium-responsive element binding 1 (creb, pcreb), early-growth response protein 1 (egr 1), brain derived neurotrophic factor (BDNF), drebrin and postsynaptic density-95 (PSD-95). These results may indicate genetic determination of synaptic plasticity-related mechanisms relevant for the molecular events mediating hippocampal information processing and storage. Data presented herein highlight the importance of careful selection of the mouse strain for studies of synaptic plasticity.