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Age‐associated changes in Ca 2+ ‐dependent processes: Relation to hippocampal synaptic plasticity
Author(s) -
Foster Thomas C.,
Norris Christopher M.
Publication year - 1997
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/(sici)1098-1063(1997)7:6<602::aid-hipo3>3.0.co;2-g
Subject(s) - synaptic plasticity , neuroscience , metaplasticity , synaptic scaling , nonsynaptic plasticity , homeostatic plasticity , synaptic fatigue , synaptic augmentation , hippocampal formation , homosynaptic plasticity , homeostasis , hippocampus , neuroplasticity , long term potentiation , neuropathology , psychology , chemistry , biology , inhibitory postsynaptic potential , excitatory postsynaptic potential , medicine , microbiology and biotechnology , biochemistry , receptor , disease
Altered calcium (Ca 2+ ) homeostasis is thought to play a key role in aging and neuropathology resulting in memory deficits. Several forms of hippocampal synaptic plasticity are dependent on Ca 2+ , providing a potential link between altered Ca 2+ homeostasis and memory deficits associated with aging. The current study reviews evidence for Ca 2+ dysregulation during aging which could interact with Ca 2+ ‐dependent synaptic plasticity. The authors suggest that changes in Ca 2+ regulation could adjust the thresholds for synaptic modification, favoring processes for depression of synaptic strength during aging. Hippocampus 1997;7:602–612.