Article

Activation of A1 and A2 noradrenergic neurons in response to running in the rat.

Laboratory of Exercise Biochemistry, University of Tsukuba, Graduate School of Comprehensive Human Sciences, 1-1-1 TennĂ´dai, Tsukuba, Ibaraki 305-8574, Japan.
Neuroscience Letters (impact factor: 2.11). 03/2006; 395(1):46-50. DOI:10.1016/j.neulet.2005.10.053 pp.46-50
Source: PubMed

ABSTRACT Since running accompanied with blood lactate accumulation stimulates the release of adrenocorticotropic hormone (ACTH), running above the lactate threshold (LT) acts as stress (running stress). To examine whether A1/A2 noradrenergic neurons that project to the hypothalamus activate under running stress, c-Fos immunohistochemistry was used to compare the effects of running with or without stress response on A1/A2 noradrenergic neurons. Blood lactate and plasma ACTH concentrations significantly increased in the running stress group, but not in the running without stress response and control groups, confirming different physiological impacts between different intensity of running with or without stress. Running stress markedly increased c-Fos accumulation in the A1/A2 noradrenergic neurons. Running without stress response also induced a significant increase in c-Fos expression in the A1/A2 noradrenergic neurons, and the percentage of the increase was smaller than that of running stress. The extent of c-Fos expression in the A1/A2 noradrenergic neurons correlates with exercise intensity, signifying that this neuronal activation is running speed-dependent. We thus suggest that A1/A2 noradrenergic neurons are activated in response to not only running stress, but also to other physiological running, enhanced by non-stressful running. These findings will be helpful in studies of specific neurocircuits and in identifying their functions in response to running at different intensities.

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Keywords

A1/A2 noradrenergic neurons
 
A1/A2 noradrenergic neurons correlates
 
ACTH
 
adrenocorticotropic hormone
 
Blood lactate
 
blood lactate accumulation stimulates
 
c-Fos accumulation
 
c-Fos expression
 
c-Fos immunohistochemistry
 
control groups
 
different intensities
 
different intensity
 
different physiological impacts
 
hypothalamus activate
 
lactate threshold
 
non-stressful
 
plasma ACTH concentrations
 
running stress group
 
specific neurocircuits
 
stress response