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. 2012 Feb;112(4):535-41.
doi: 10.1152/japplphysiol.00306.2011. Epub 2011 Dec 1.

Acute running stimulates hippocampal dopaminergic neurotransmission in rats, but has no influence on brain-derived neurotrophic factor

Affiliations

Acute running stimulates hippocampal dopaminergic neurotransmission in rats, but has no influence on brain-derived neurotrophic factor

Maaike Goekint et al. J Appl Physiol (1985). 2012 Feb.

Abstract

Hippocampal brain-derived neurotrophic factor (BDNF) protein is increased with exercise in rats. Monoamines seem to play a role in the regulation of BDNF, and monoamine neurotransmission is known to increase with exercise. The purpose of this study was to examine the influence of acute exercise on monoaminergic neurotransmission and BDNF protein concentrations. Hippocampal microdialysis was performed in rats that were subjected to 60 min of treadmill running at 20 m/min or rest. Two hours postexercise, the rats were killed, and the hippocampus was dissected. In experiments without microdialysis, hippocampus and serum samples were collected immediately after exercise. Exercise induced a twofold increase in hippocampal dopamine release. Noradrenaline and serotonin release were not affected. Hippocampal BDNF levels were not influenced, whether they were measured immediately or 2 h after the exercise protocol. Serum BDNF levels did not change either, but serum BDNF was negatively correlated to peripheral corticosterone concentrations, indicating a possible inhibitory reaction to the stress of running. Sixty minutes of exercise enhances dopamine release in the hippocampus of the rat in vivo. However, this increase is not associated with changes in BDNF protein levels immediately nor 2 h after the acute exercise bout. An increased corticosterone level might be the contributing factor for the absence of changes in BDNF.

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Figures

Fig. 1.
Fig. 1.
Experimental protocols for the different groups. In rats undergoing microdialysis, 120 min of baseline sampling were followed by 60 min of experimental intervention (EM, n = 7: running at 20 m/min; CM, n = 6: rest) and again 120 min at rest. Rats were killed after the 120 min of recovery following the experimental intervention. Rats of E0 and C0 did not undergo microdialysis. They were at rest on the treadmill for 120 min, followed by 60 min of experimental intervention (E0, n = 6: running at 20 m/min; C0, n = 6: rest). Immediately afterwards, rats were killed. C, control group; E, experimental group; M, microdialysis; 0, no microdialysis; BDNF, brain-derived neurotrophic factor.
Fig. 2.
Fig. 2.
Changes in extracellular dopamine (DA; A), noradrenaline (NA; B), and serotonin (5-HT; C) concentrations in the hippocampus following 60-min exercise at 20 m/min. The average concentration of 6 microdialysis samples before treadmill exercise (Ex) was taken as the baseline and was defined as 100%. Values are means ± SE (%baseline values). For DA levels, a significant difference was present between the EM and CM group (P < 0.01). Within the experimental group, DA release increased during exercise compared with baseline (*P < 0.05; **P < 0.01). For NA and 5-HT levels, no significant differences were present between the EM and CM group. Within the experimental group, no changes were detected in the release of these transmitters with exercise.
Fig. 3.
Fig. 3.
Hippocampal (top) and serum (bottom) BDNF content immediately (C0-E0) or 2 h (CM-EM) following the experimental protocol. Values are means ± SE in pg/mg (hippocampal homogenates) and ng/ml (serum). No significant differences were found between the experimental (60 min of running at 20 m/min) and the sedentary control group.
Fig. 4.
Fig. 4.
Serum corticosterone concentration immediately following the experimental protocol in the C0 and E0 group. Values are means ± SE (ng/ml). The corticosterone level after 60 min of running at 20 m/min was significantly higher compared with that of the sedentary control group (*P = 0.007).

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