enhancing hippocampal neuronal numbers in morphine-dependent rats by voluntary exercise through a brain-derived neurotrophic factor- mediated mechanism

Background: exposure to morphine decreases neurogenesis in the hippocampus. recent studies have shown that voluntary running decreases the severity of anxiety behaviors and cognitive deficits, and increased synaptic plasticity in morphine-dependent rats. objectives: this study aimed to investigate whether the morphine dependence-induced attenuation of hippocampal neuron number in rats would be reversed by voluntary running through a brain-derived neurotrophic factor (bdnf)-mediated mechanism. materials and methods: the rats were received injections of 10 mg/kg of morphine twice a day over ten days of voluntary running. a specific antagonist of bdnf action (trkb-igg) was used to block the hippocampal bdnf action during the study period; cytochrome c (cyt c) was used as the control drug. results: we found that chronic exposure to morphine had decreased the number of dentate gyrus neurons in sedentary rats receiving cyt c or igg in comparison to the control rats (p < 0.05). moreover, exercise groups receiving saline or morphine showed an increase in the number of neurons following ten days running; blocking the bdnf action with trkb-igg fully inhibited this effect (both, p = 0.0001). conclusions: this study demonstrates that that voluntary exercise can ameliorate the attenuation of hippocampal neuron number induced by morphine dependence through a bdnf-mediated mechanism. thus, physical activity might have a potential role in ameliorating chronic morphine-induced neuronal changes in the hippocampus.