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Volume 3
Journal of Neurology and Clinical Neuroscience
Neurosurgery 2019 & Neuroimmunology 2019
May 22-23, 2019
Neurosurgery and Neurological Surgeons
Neuroscience and Neuroimmunology
May 22-23, 2019 London, UK
6
th
Annual Meeting on
9
th
Global Summit on
&
J Neurol Clin Neurosci, Volume 3
Strain differences in sympathetic neurotransmission in spleens of rats subjected to
reduced sympathetic tone
Samuel Perez
Washington Adventist University, USA
S
enescence 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 age- related 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 (Adrenergic
Receptor) expression, splenocyte c-AMP (Cyclic adenosine monophosphate) 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 low- grade systemic inflammation.
Biography
Samuel Perez is currently working as an assistant professor in Washington Adventist University, Maryland. He acheived his PH.D in
the area of Neurophysiology/Neuroimmunology at Loma Linda University School of Medicine, California. Sam D Perez obtained the
degree of master’s in Molecular Physiology at Loma Linda University. His scientific research interest includes: Study the effects of
neuroprotective micronutrients on learning and memory function in animal models using molecular biology tools and animal models to
understand neuroimmune mechanisms of cell protection and many more.
sperez@wau.edu