Abstract
Age-associated memory impairments may result as a consequence of neuroinflammatory induction of intracellular calcium (Ca+2) dysregulation. Altered L-type voltage-dependent calcium channel (L-VDCC) and ryanodine receptor (RyR) activity may underlie age-associated learning and memory impairments. Various neuroinflammatory markers are associated with increased activity of both L-VDCCs and RyRs, and increased neuroinflammation is associated with normal aging. In vitro, pharmacological blockade of L-VDCCs and RyRs has been shown to be anti-inflammatory. Here, we examined whether pharmacological blockade of L-VDCCs or RyRs with the drugs nimodipine and dantrolene, respectively, could improve spatial memory and reduce age-associated increases in microglia activation. Dantrolene and nimodipine differentially attenuated age-associated spatial memory deficits but were not anti-inflammatory in vivo. Furthermore, RyR gene expression was inversely correlated with spatial memory, highlighting the central role of Ca+2 dysregulation in age-associated memory deficits.
Original language | English (US) |
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Pages (from-to) | 10-18 |
Number of pages | 9 |
Journal | Neuroscience |
Volume | 280 |
DOIs | |
State | Published - Nov 1 2014 |
Externally published | Yes |
Keywords
- Aging
- Calcium
- L-type voltage-dependent calcium channel
- Memory
- Microglia
- Ryanodine receptor
ASJC Scopus subject areas
- General Neuroscience