Brain norepinephrine changes with simulated weightlessness and relation to exercise training

Maintenance of nervous system function during periods of a deconditioning syndrome is important to prevent diminished psychological/behavioral, and physiological function observed during periods of bed rest, physical inactivity, and weightlessness. A main neurotransmitter is norepinephrine (NE), and its regulation yields insight into nervous system function. This research tested the hypotheses that, 1) deconditioning syndrome induced by simulated weightlessness of 9 days via the head-down tilt (HDT) model results in a blunted noradrenergic turnover rate in selected brain tissue and, 2) that exercise training acts as a countermeasure for these changes in noradrenergic activity. Male Sprague-Dawley rats (3 months, n = 60) were divided into either a HDT (HDT, n = 20), cage control (CAGE-CN, n = 20) or an exercise trained HDT (HDT-EX, n = 20) group. Each group was further subdivided into a saline (n = 10) or alpha-methyl-tyrosine (AM, n = 10) (200 mg/kg) injected subgroup. Animals in the HDT groups were tail suspended in a 30 degrees head-down tilt position for 9 days. Norepinephrine turnover was determined 3 h following administration of saline or alpha-methyl-para-tyrosine. The NE turnover rate (ng gm(-1) x h(-1)) for the CN, HDT, and HDT-EX groups, respectively, were as follows: locus coeruleus, 63 +/- 33, *134 +/- 65, 85 +/- 61; hypothalamus, 195 +/- 50, *47 +/- 47; *93 +/- 34; cerebellum, 10 +/- 18, *65 +/- 15, *53 +/- 19; cerebral cortex, 6 +/- 20, *28 +/- 15, *68 +/- 22. (*Denotes significant difference from the control group at the p < or = 0.05 level of significance; +denotes significant difference from the HDT group at the p < or = 0.05 level of significance.) These findings suggest that: 1) norepinephrine turnover rate adapts in a tissue-specific manner following a 9-day tail suspension, 2) increased norepinephrine turnover rates and norepinephrine tissue content in the HDT group are consistent with neural adaptation to a chronic stress response.