Aging and stress delay the onset of acute inflammation and subsequently healing of injured tissues. After spinal cord injury (SCI), repair and regeneration of damaged tissues, both CNS and peripheral tissues (e.g., surgical incisions, pressure sores), is dependent on inflammatory processes. As medical care has improved, the life expectancy of spinal injured individuals has increased to a level that is consistent with the able- bodied population. As such, SCI survivors must learn to cope with the physiological stress as disability, as well as the physiological challenges of aging. In the present proposal, we will address the interrelationship between aging, stress, and wound healing in a clinically relevant model of SCI. It is the major hypothesis of this proposal that aging and the stress associated with SCI will suppress inflammatory processes resulting in delayed or incomplete wound healing in the CNS. In this proposal, we will define baseline parameters of hypothalamic-pituitary-adrenal (HPA) axis activation (measurement of plasma CORT and ACTH) as a function of time post-injury in three ages of mice (young, adult, aged). These data will define the peak and duration of HPA activation, which can then be correlated with measures of acute inflammation in the spinal cord (e.g., cellularity, cytokines, chemokines). Morphometric analysis of immunohistochemically-stained injured spinal cord sections will allow us to determine how altered immunological processes affect wound healing in the CNS. Together, these analyses will help us to deter define the effects of aging and stress on repair and/or regeneration of the injured spinal cord.
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