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Enhanced CaMKII activity and spatial cognitive function in SAMP6 mice.

Eiki Takahashi¹, Kimie Niimi, Chitoshi Itakura

¹Research Resources Center, RIKEN Brain Science Institute, Saitama, Japan. etakahashi@brain.riken.jp

Behavioral Neuroscience

|June 3, 2009

Summary

Senescence-accelerated mouse prone 6 (SAMP6) mice show enhanced spatial learning and memory. This is linked to increased alpha calcium/calmodulin-dependent protein kinase II (CaMKII) activity and NMDA receptor NR2B subunit expression in the hippocampus.

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Area of Science:

Neuroscience
Aging Research
Molecular Biology

Background:

Senescence-accelerated mouse prone 6 (SAMP6) mice display altered cognitive function compared to senescence-accelerated mouse resistance 1 (SAMR1) mice.
The NMDA receptor NR2B subunit (NR2B) and alpha calcium/calmodulin-dependent protein kinase II (CaMKII) are implicated in memory and plasticity.

Purpose of the Study:

To investigate the relationship between CaMKII activity and spatial learning in SAMP6 mice.
To explore the role of the NR2B/CaMKII signaling pathway in cognitive function during aging.

Main Methods:

Western blot analysis to assess protein phosphorylation levels in the hippocampus.
Behavioral tests including object location and delayed spatial win-shift eight-arm radial-maze to evaluate spatial learning and memory.

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Main Results:

SAMP6 mice exhibited increased Thr286 phosphorylation of CaMKII and Ser831 phosphorylation of glutamate receptor 1 (a CaMKII substrate) in the hippocampus compared to SAMR1 mice.
SAMP6 mice demonstrated superior hippocampal-dependent spatial memory formation in both behavioral tests.

Conclusions:

Increased CaMKII activity in SAMP6 mice is associated with enhanced spatial learning and memory.
The NR2B/CaMKII signaling pathway plays a significant role in modulating cognitive function in aging SAMP6 mice.