Why the brain slows down when we age

February 2, 2012

Age-dependent hypoexcitability of hippocampal CA1 pyramidal neurons (CA1-PCs). Aged mice are shown in gray. (credit: Andrew D. Randall et al./Neurobiology of Aging)

New findings by neuroscientists at the University of Bristol reveal why the brain may become less able to function as we grow older.

In mice studies, the research identified a novel cellular mechanism (sodium channels) underpinning changes to the activity of neurons, which may underlie cognitive decline during normal healthy aging.

The researchers recorded electrical signals in single cells of the hippocampus, a structure with a crucial role in cognitive function to measure “neuronal excitability” — how easy it is to produce brief but very large electrical signals called action potentials (APs).

They found that in the aged brain, it is more difficult to make hippocampal neurons generate action potentials, due to changes to the activation properties of membrane proteins called sodium channels. These mediate the rapid upstroke of the action potential by allowing a flow of sodium ions into neurons.

“Also, by identifying sodium channels as the likely culprit for this reluctance to produce action potentials, our work even points to ways in which we might be able to modify age-related changes to neuronal excitability, and by inference, cognitive ability,” said Professor Randall, University of Bristol Professor in Applied Neurophysiology.

“The mechanism underlying this change in sodium-channel gating properties remains to be explored,” the researchers say.

Ref.: Andrew D. Randall, Clair Booth, Jon T. Brown, Age-related changes to Na+ channel gating contribute to modified intrinsic neuronal excitability, Neurobiology of Aging, 2012; [DOI:10.1016/j.bbr.2011.03.031] (in press)