Caloric restriction does not offset age-associated changes in the biophysical properties of motoneurons

Age-associated changes in neuromuscular function may be due to a loss of motor neurons as well as changes in their biophysical properties. Neuronal damage imposed by reactive oxygen species may contribute to age-related deficits in CNS function. Thus we hypothesized that aging would alter the functional properties of motoneurons and that caloric-restriction would offset these changes. Intracellular recordings were made from lumbar motoneurons of old Fisher Brown Norway (FBN) fed ad libitum (oldAL, 30.8+/-1.3 mo) or on a fortified calorie-restricted diet from 14 wk of age (oldCR, 31.0+/-1.8 mo). Basic and rhythmic firing properties recorded from these aged motoneurons (MNs) were compared with properties recorded from young FBN controls (young, 8.4+/-4.6 mo). Compared with young MNs, old MNs had a 104% greater (P<0.001) afterhyperpolarization potential (AHP), a 21.1% longer AHP half-decay time (P<0.05), 28.7% lower rheobase (P<0.001), 49.7% greater (P<0.001) input resistance, 21.1% (P<0.0001) less spike frequency adaptation, lower minimal (30.2%, P<0.0001) and maximal (16.7%, P<0.0001) steady-state firing frequencies, a lower (35.5%, P<0.0001) frequency-current slope, and an increased incidence of persistent inward current. Because basic properties became more diverse in old MNs and the slope of the frequency-current relationship, which is normally similar for high- and low-threshold MNs, was lower in the old group, we conclude that aging alters the biophysical properties of MNs in a fashion that cannot be simply attributed to a loss of high-threshold MNs. Surprisingly, caloric restriction, which is known to attenuate aging-associated changes in hindlimb muscles, had no effect on the progress of aging in the innervating MNs.