Neural plasticity is impaired in cold-exposed hippocampal slices from senescent but not from age-matched presenescent F344 rats.

Near the end of their natural life, many mammals enter a terminal state identifiable by a rapid loss of body weight resulting from hypophagia. This study extends characterization of this senescent state by comparing viability of metabolic mechanisms supporting neural plasticity in hippocampal slices from 24 to 30 month old senescent and age-matched presenescent (body-weight stable) F344 male rats. Half of the slices from each rat were incubated at 22-23 degrees C, and half were immersed in cool incubation medium (12-15 degrees C) immediately after slicing and allowed to passively warm to room temperature over approximately 50 min to impose a cold stressor on recovery mechanisms. Following incubation, CA1 pyramidal cell population spike (PS) amplitudes were measured before and after tetanus. In slices incubated at 22-23 degrees C, the 221.0+/-24.2 % increase in PS amplitude following tetanus in seven slices from five senescent rats was not significantly different from the 202.5+/-23.8% increase in six slices from five age-matched presenescent rats. In contrast, in cold-exposed slices, the 133.8+/-13.1% increase in PS amplitude following tetanus in 14 slices from 10 senescent rats was significantly smaller (p<0.05) than the 184.7+/-10.2% increase in 13 slices from seven age-matched presenescent rats. This smaller PS enhancement in senescent rats cannot be attributed to weight loss because robust potentiation was induced in cold-exposed slices from five food-restricted presenescent rats having a weight loss comparable to their senescent counterparts. Thus, the blunted enhancement observed in cold-exposed slices appears to be a characteristic of senescence.