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.