Hippocampally-dependent trace eyeblink conditioning has been shown to
be affected by aging. Aging animals take more trials to acquire the as
sociation and are more likely to be unable to learn the task. Hippocam
pal neurons show decreased post-burst afterhyperpolarizations (AHPs) a
nd less accomodation after conditioning, in a time-dependent fashion w
hich may relate to the role of hippocampus in learning consolidation.
CA1 neurons in aging rabbits show increased AHPs and more accomodation
, i.e., they are less excitable, and larger calcium action potentials.
These age-related changes may underlie the learning deficits in aging
rabbits. The lipophylic calcium channel blocker nimodipine reduces th
e AHP, accomodation and calcium action potential at low concentrations
in aging but not young CA1 neurons. Nimodipine also enhances learning
rate in a variety of tasks, including eyeblink conditioning, in aging
but not young animals and humans. Altered calcium handling by neurons
of aging mammals is a striking change, is pharmacologically manipulab
le, and may be an important factor in altered learning and cognitive a
bilities in the aging.