Open AccessCalcium homeostasis and modulation of synaptic plasticity in the aged brain
Author(s) -
Foster Thomas C.
Publication year - 2007
Publication title -
aging cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.103
H-Index - 140
eISSN - 1474-9726
pISSN - 1474-9718
DOI - 10.1111/j.1474-9726.2007.00283.x
Subject(s) - biology , intracellular , neuroscience , synaptic plasticity , homeostasis , synaptic scaling , homeostatic plasticity , cytosol , hippocampus , calcium signaling , metaplasticity , neuroplasticity , senescence , calcium in biology , microbiology and biotechnology , receptor , biochemistry , enzyme
Summary The level of intracellular Ca 2+ plays a central role in normal and pathological signaling within and between neurons. These processes involve a cascade of events for locally raising and lowering cytosolic Ca 2+ . As the mechanisms for age‐related alteration in Ca 2+ dysregulation have been illuminated, hypotheses concerning Ca 2+ homeostasis and brain aging have been modified. The idea that senescence is due to pervasive cell loss associated with elevated resting Ca 2+ has been replaced by concepts concerning changes in local Ca 2+ levels associated with neural activity. This article reviews evidence for a shift in the sources of intracellular Ca 2+ characterized by a diminished role for N‐methyl‐D‐aspartate receptors and an increased role for intracellular stores and voltage‐dependent Ca 2+ channels. Physiological and biological models are outlined, which relate a shift in Ca 2+ regulation with changes in cell excitability and synaptic plasticity, resulting in a functional lesion of the hippocampus.