Age-related changes in the synaptic plasticity of rat superior cervical ganglia

Abstract

A few seconds of tetanic preganglionic stimulation of rat sympathetic ganglia results in potentiation of cholinergic synaptic transmission lasting several hours. However, ganglia from aged (28–32 months) rats did not develop as much potentiation as did ganglia from young (3–6 months) rats. This potentiation appears to decay exponentially but in two phases. The early component decays in 15 minutes, a time course consistent with the phenomenon of post-tetanic potentiation (PTP). The later component decays over several hours and is a form of long-term potentiation (LTP). A double exponential decay model was employed to quantitatively resolve the decay of potentiation and allow quantitative comparison of the decay parameters in both aged and young rats. It is clear that the magnitude and duration of PTP was the same in both age groups. However both the magnitude and decay time-constant for LTP were 30–50% smaller in the aged group of rats. Several agents which mimic cyclic AMP or stimulate cyclic AMP production in the ganglion enhance nicotinic transmission for several hours. However, these agents, 8-bromo cAMP, forskolin, isoproterenol, and secretin were equally effective in potentiating transmission in ganglia from both young and aged rats. Previous studies demonstrated that stimulus induced LTP and cyclic AMP induced potentiation was the result of enhanced release of acetylcholine (ACh) and not from increased postsynaptic responsiveness. Presumably these agents act through the same pathway and by the same mechanism that generates LTP following preganglionic tetany. These observations demonstrate that there is a selective age-dependent decline in the capacity for sympathetic ganglia to generate long-term changes in synaptic efficacy. It is hypothesized that impaired ganglionic LTP in aged animals results from a decrease in the evoked co-release of an as yet unidentified preganglionic terminal modulator.