Altered synaptic dynamics during normal brain aging

Ricardo Mostany, James E. Anstey, Kerensa L. Crump, Bohumil Maco, Graham Knott, Carlos Portera-Cailliau

Research output: Contribution to journalArticlepeer-review

98 Scopus citations

Abstract

What is the neuroanatomical basis for the decline in brain function that occurs during normal aging? Previous postmortem studies have blamed it on a reduction in spine density, though results remain controversial and spine dynamics were not assessed.Weused chronic in vivo two-photon imaging of dendritic spines and axonal boutons in somatosensory cortex for up to 1 year in thy1 GFP mice to test the hypothesis that aging is associated with alterations in synaptic dynamics. We find that the density of spines and en passant boutons (EPBs) in pyramidal cells increases throughout adult life but is stable between mature (8-15 months) and old (>20 months) mice. However, new spines and EPBs are two to three times more likely to be stabilized over 30 d in old mice, although the long-term retention (over months) of stable spines is lower in old animals. In old mice, spines are smaller on average but are still able to make synaptic connections regardless of their size, as assessed by serial section electron microscopy reconstructions of previously imaged dendrites. Thus, our data suggest that age-related deficits in sensory perception are not associated with synapse loss in somatosensory cortex (as might be expected) butwithalterations in the sizeandstability of spinesandboutonsobservedin this brain area.Thechangeswedescribeherelikely result inweaker synapses that are less capable of short-term plasticity in aged individuals, and therefore to less efficient circuits.

Original languageEnglish (US)
Pages (from-to)4094-4104
Number of pages11
JournalJournal of Neuroscience
Volume33
Issue number9
DOIs
StatePublished - Feb 27 2013
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint

Dive into the research topics of 'Altered synaptic dynamics during normal brain aging'. Together they form a unique fingerprint.

Cite this