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Updated: Feb 15, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
Published on: March 23, 2011
Altered function of neuronal L-type calcium channels in ageing and neuroinflammation: Implications in age-related
Sheeja Navakkode1, Chao Liu1, Tuck Wah Soong2
1Dept. of Physiology, Yong Loo Lin School of Medicine, Singapore; Neurobiology/Ageing Program, Centre for Life Sciences, National University of Singapore, Singapore.
Abstract:
The rapid developments in science have led to an increase in human life expectancy and thus, ageing and age-related disorders/diseases have become one of the greatest concerns in the 21st century. Cognitive abilities tend to decline as we get older. This age-related cognitive decline is mainly attributed to aberrant changes in synaptic plasticity and neuronal connections. Recent studies show that alterations in Ca2+ homeostasis underlie the increased vulnerability of neurons to age-related processes like cognitive decline and synaptic dysfunctions. Dysregulation of Ca2+ can lead to dramatic changes in neuronal functions. We discuss in this review, the recent advances on the potential role of dysregulated Ca2+ homeostasis through altered function of L-type voltage gated Ca2+ channels (LTCC) in ageing, with an emphasis on cognitive decline. This review therefore focuses on age-related changes mainly in the hippocampus, and with mention of other brain areas, that are important for learning and memory. This review also highlights age-related memory deficits via synaptic alterations and neuroinflammation. An understanding of these mechanisms will help us formulate strategies to reverse or ameliorate age-related disorders like cognitive decline.
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