Speaker Biography

Sam Perez

Washington Adventist University , USA

Title: Strain differences in sympathetic neurotransmission in spleens of rats subjected to reduced sympathetic tone

Biography:

Abstract:

Senescence of innate and adaptive responses and low-grade inflammation(inflammaging) hallmarks normal aging, which increases vulnerability to infectious diseases, autoimmunity and cancer. In normal aging, sympathetic dysregulation contributes to the dysregulation of innate and adaptive immunity and inflammaging. Sympathetic innervation of immune cells in secondary immune organs regulates immune responses. Different profiles of sympathetic signaling during aging may bring about different effects on neurotransmission in immune cells that may lead to immunity variation in senescence. We investigated whether increased sympathetic nerve activity (SNA) in the aging spleen contributes to agerelated sympathetic neuropathy and altered neurotransmission in splenic lymphocytes of two strain of rats of strikingly different sympathetic activation and behavior profiles. To answer this question, we injected 15 month-old rats, of either strain, 0, 0.5 or 1.5 μg/kg/day rilmenidine intraperitoneally, for 90 days to lower sympathetic tone. Untreated young and age-matched rats controlled for effects of age.  We found that in Fischer 344 (F344) rats, an age-related increase in sympathetic tone and sympathetic dysfunction in beta-adrenergic receptor (AR) signaling of splenic lymphocytes contribute to immune senescence. In the much longer-lived Brown-Norway (BN) rats, we observed that elevated SNA in the aging BN rat spleen does not contribute significantly to sympathetic neuropathy or the aging-induced impairment of canonical β-AR signal transduction. Despite the rilmenidine-induced increase in β-AR expression, splenocyte c-AMP production was comparable with age-matched controls, thus dampening nerve activity had no effect on receptor coupling to adenylate cyclase. Understanding how aging differentially affects neuroimmune regulation in healthy aging rodent of different strain models can help us formulate strategies to improve health in aging populations that are most vulnerable to immunosenescence and lowgrade systemic inflammation.