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Calcium homeostasis in aged neurones
1Bogomoletz Institute of Physiology, Kiev, Ukraine.
Life Sciences
|January 1, 1996
Summary
Aging significantly alters neuronal calcium homeostasis, increasing resting calcium levels and prolonging stimulus-evoked signals. This suggests aged neurons have a reduced capacity to manage calcium, potentially increasing their vulnerability.
Area of Science:
- Neuroscience
- Cell Biology
- Aging Research
Background:
- Cytoplasmic calcium homeostasis is crucial for neuronal function.
- Age-related changes in neuronal physiology are not fully understood.
- Calcium dysregulation is implicated in neurodegenerative processes.
Purpose of the Study:
- To investigate age-associated alterations in cytoplasmic calcium homeostasis in neurons.
- To compare calcium handling in peripheral and central neurons across different age groups.
- To elucidate the impact of aging on neuronal calcium signaling dynamics.
Main Methods:
- Isolation of peripheral and central neurons from rats of different ages (neonatal, adult, old).
- Preparation of cerebellar slices from adult and old mice.
- Measurement of cytoplasmic calcium concentration ([Ca2+]i) using indo-1/fura-2 microfluorimetry.
- Assessment of depolarization-induced calcium transients and calcium release from endoplasmic reticulum stores.
Main Results:
- Senile neurons exhibited significantly higher resting [Ca2+]i.
- Old neurons showed decreased amplitudes, prolonged rising phases, and slower recovery of [Ca2+]i transients upon depolarization.
- Calcium release from endoplasmic reticulum stores diminished in old central neurons but not peripheral neurons.
Conclusions:
- Neuronal aging is associated with significant disruptions in calcium homeostasis mechanisms.
- These changes result in elevated resting [Ca2+]i and prolonged calcium signals.
- Aged neurons demonstrate impaired calcium load handling, potentially increasing their susceptibility to calcium toxicity.