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The basal concentrations of extracellular Zn 2+ and intracellular Zn 2+ , which are approximately 10 nM and 100 pM, respectively, in the brain, are markedly lower than those of extracellular Ca 2+ (1.3 mM) and intracellular Ca 2+ (100 nM), respectively, resulting in much less attention paid to Zn 2+ than to Ca 2+ . However, intracellular Zn 2+ dysregulation, which is closely linked with glutamate- and amyloid β-mediated extracellular Zn 2+ influx, is more critical for cognitive decline and neurodegeneration than intracellular Ca 2+ dysregulation. It is estimated that the age-dependent increase in the basal concentration of extracellular Zn 2+ in the hippocampus plays a key role in cognitive decline and neurodegeneration. The characteristics of extracellular Zn 2+ influx in the hippocampus may be modified age-dependently, probably followed by modification of intracellular Zn 2+ buffering that is closely linked with age-related cognitive decline and neurodegeneration. Reduction of intracellular Zn 2+ -buffering capacity may be linked with the pathophysiology of progressive neurodegeneration such as Alzheimer's disease. This paper deals with age-dependent modification of intracellular Zn 2+ buffering in the hippocampus and its impact. On the basis of the estimated impact, we propose a potential defense strategy against Zn 2+ -mediated neurodegeneration, i.e., metallothionein induction in the hippocampus.

Age-Dependent Modification of Intracellular Zn<sup>2+</sup> Buffering in the Hippocampus and Its Impact