Brett Melanson1, Thomas Lapointe1, Francesco Leri2. 1. Department of Psychology and Collaborative Neuroscience Program, University of Guelph, 50 Stone Road East, Guelph, ON, N1G 2W1, Canada. 2. Department of Psychology and Collaborative Neuroscience Program, University of Guelph, 50 Stone Road East, Guelph, ON, N1G 2W1, Canada. fleri@uoguelph.ca.
Abstract
RATIONALE: There is evidence that hypoglycemia, a metabolic stressor, can negatively impact mood and motivation, and can interact with other stressors to potentiate their effects on behavior and physiology. OBJECTIVES/ METHODS: The current study in male Sprague-Dawley rats explored the interaction between impaired glucose metabolism induced by 0, 200, or 300 mg/kg 2-deoxy-D-glucose (2-DG) and a psychophysical stressor induced by forced swimming stress (FSS; 6 sessions, 10 min/session). The endpoints of interest were blood glucose levels, progressive behavioral immobility, and saccharin preference (2-bottle choice test). Furthermore, it was investigated whether pre-treatment with 0, 10, or 20 mg/kg ketamine could modify the interaction between 2-DG and FSS on these endpoints. RESULTS: It was found that 2-DG increased blood glucose levels equally in all experimental groups, accelerated the immobile response to FSS, and suppressed saccharin preference 1 week following termination of stress exposure. As well, pre-treatment with ketamine blocked the effects of combined 2-DG and FSS on immobility and saccharin preference without affecting blood glucose levels and produced an anti-immobility effect that was observed during a drug-free test swim 1 week following administration. CONCLUSIONS: Overall, these findings demonstrate that impaired glucose metabolism can potentiate the effects of a psychophysical stressor, and that this interaction can be modulated pharmacologically by ketamine.
RATIONALE: There is evidence that hypoglycemia, a metabolic stressor, can negatively impact mood and motivation, and can interact with other stressors to potentiate their effects on behavior and physiology. OBJECTIVES/ METHODS: The current study in male Sprague-Dawley rats explored the interaction between impaired glucose metabolism induced by 0, 200, or 300 mg/kg 2-deoxy-D-glucose (2-DG) and a psychophysical stressor induced by forced swimming stress (FSS; 6 sessions, 10 min/session). The endpoints of interest were blood glucose levels, progressive behavioral immobility, and saccharin preference (2-bottle choice test). Furthermore, it was investigated whether pre-treatment with 0, 10, or 20 mg/kg ketamine could modify the interaction between 2-DG and FSS on these endpoints. RESULTS: It was found that 2-DG increased blood glucose levels equally in all experimental groups, accelerated the immobile response to FSS, and suppressed saccharin preference 1 week following termination of stress exposure. As well, pre-treatment with ketamine blocked the effects of combined 2-DG and FSS on immobility and saccharin preference without affecting blood glucose levels and produced an anti-immobility effect that was observed during a drug-free test swim 1 week following administration. CONCLUSIONS: Overall, these findings demonstrate that impaired glucose metabolism can potentiate the effects of a psychophysical stressor, and that this interaction can be modulated pharmacologically by ketamine.
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