Differential rescue of spatial memory deficits in aged rats by L-type voltage-dependent calcium channel and ryanodine receptor antagonism

S. C. Hopp, H. M. D'Angelo, S. E. Royer, R. M. Kaercher, L. Adzovic, G. L. Wenk

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

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 languageEnglish (US)
Pages (from-to)10-18
Number of pages9
JournalNeuroscience
Volume280
DOIs
StatePublished - Nov 1 2014
Externally publishedYes

Keywords

  • Aging
  • Calcium
  • L-type voltage-dependent calcium channel
  • Memory
  • Microglia
  • Ryanodine receptor

ASJC Scopus subject areas

  • Neuroscience(all)

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