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Abstract

Stimulation of the sympathetic nervous system (SNS) and the release of norepinephrine (NE) is a powerful feature of the acute stress response that is adaptive when the response is acute and constrained. If SNS activation is frequent or excessive, however, it can contribute to negative health consequences including “metabolic syndrome” and immunosuppression. We recently reported that sedentary rats exposed to a well-characterized acute stressor (uncontrollable tailshock) excessively activate the SNS leading to depletion of NE below basal levels in some peripheral tissues. NE depletion specifically in the spleen suppresses the in vivo immunoglobulin response to an antigenic protein challenge (keyhole limpet hemocyanin, αKLH immunoglobulin (Ig)). Regular moderate physical activity (voluntary wheel running) buffers a wide array of negative consequences of acute stressor exposure including splenic NE depletion and αKLH Ig suppression. In the current chapter we will present the hypothesis that adaptations in the central sympathetic neurocircuit produced by physical activity constrain excessive stress-induced SNS responses, thereby preventing splenic NE depletion and αKLH Ig and anti-tetanus toxoid Ig suppression in physically active stressed rats.

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Fleshner, M., Kennedy, S.L., Johnson, J.D., Day, H.E., Greenwood, B.N. (2009). Exercise and Stress Resistance: Neural-Immune Mechanisms. In: Siegel, A., Zalcman, S.S. (eds) The Neuroimmunological Basis of Behavior and Mental Disorders. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-84851-8_6

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