Reactive synaptogenesis in hippocampal area CA1 of aged and young adult rats

Selective lesions that result in a partial loss of neuronal input appear to signal residual, undamaged inputs to sprout and replace synaptic connections that have been lost. Previous investigations have compared this process of reactive synaptogenesis in young and old animals in the hippocampal dentate gyrus and have demonstrated that the aged brain has a diminished capacity for reinnervation following massive denervation of a target area. This investigation has focused on the lesion-induced plasticity of an adjacent area of the hippocampal formation, area CA1 of regio superior, in young adult and aged rats. Young adult aged Fischer 344 rates were subjected to a unilateral, intraventricular injection of kainic acid that selectively destroyed the CA3-CA4 hippocampal pyramidal neurons. Following a 2-day interoperative interval, the rats sustained an ipsilateral transection of the fimbria-fornix. Animals were killed at 4, 10, 30, and 60 days following the second transection and processed for electron microscopic analysis. Photographic montages were constructed of area CA1 extending from the alveus to the hippocampal fissure. The density of synapses, both intact and degenerating, was determined and analyzed as a function of age, days postlesion, and zone of analysis. Synaptic density decreased 30-40% contralaterally and 60-70% ipsilaterally in both aged and young adult rats. While both age groups restored synaptic density to preoperative levels, aged subjects required significantly more time. Aged rats appeared to be retarded in the initial phases of synaptic replacement. The delay in the aged animals' reactive response was not due to any differences in degeneration clearance between the age groups.