By B. N. GREENWOOD, S. KENNEDY, T. P. SMITH, S. CAMPEAU, H. E. W. DAY, AND M. FLESHNER
Department of Kinesiology and Applied Physiology, University of Colorado, Boulder, CO 80309, USA
Department of Psychology, University of Colorado, Boulder, CO 80309, USA
Center for Neuroscience, University of Colorado, Boulder, CO 80309, USA
Department of Psychology, University of Colorado, Boulder, CO 80309, USA
Center for Neuroscience, University of Colorado, Boulder, CO 80309, USA
Neuroscience 120 (2003) 269–281
Voluntary wheel running has been shown to modulate the stress responses in the from the peripheral sympathetic drive, which includes brain regions such as the locus coeruleus, the A5 cell group, and the rostral ventrolateral medulla. These brain regions project down to organs such as the adrenals and spleen. These are organs are important for the stress-induced response, releasing catecholamines into the blood system. Previous research suggests that exposure to exercise prevents the rise in norepinephrine in the blood of rats.
The current study put rats in either 6-weeks of voluntary wheel running or sedentary conditions and then had them undergo either a “control” condition (where they remained in their home cage) or began the 10, 50, or 100, 5-second inescapable tail shocks to induce a stress response. Rats were euthanized at either the baseline, 10, 50, or 100 shock exposure. Their spleens and adrenal glands were removed, flash frozen in liquid nitrogen and had their tissue catecholamine content measured. Additionally, the effects of exercise and sedentary conditions on the central sympathetic network was investigated. C-Fos protein, which is used as a neural-activation marker, was measured at baseline or after 100 tail shocks. The protein was then immunohistochemically labeled. Additionally, tyrosine hydroxylase was measured to ensure that the activity of neurons was measured only in the catecholaminergic cells in the brain regions of interest. This enzyme is essential in making norepinephrine, the neurotransmitter that the neurons use to activate the sympathetically innervated their organ targets.
In both the running and the sedentary rats, exposure to the tail-shock stressor depleted catecholamines, specifically norepinephrine, in the spleen. In the active animals, this effect was attenuated. The tail shocks showed a “dose-response,” meaning that the larger amount of tail shocks depleted more catecholamines. The same effects were measured in the adrenal glands.
c-Fos levels increased in TH-positive neurons in all brain areas after being exposed to stress. However, that increase was attenuated in exercise-exposed rats in specific brain regions that control the splenic sympathetic regulation: the LC, the intermediate to caudal A5 cell group, and the rostral ventrolateral medulla. These neurons project down as the adrenergic and noradrenergic spinally projecting sympathetic neurons to the preganglionic nerves. These then project to the organs.
These results suggest that the running condition may attenuate the splenic sympathetic activity after and during stress by reducing the input from the spinally projecting neurons. These neurons, after being exposed to exercise for 6-weeks, reduce the sympathetic excitatory drive during stress and thus there is less norepinephrine released from the spleen and adrenal nerves.
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