Abstract
Background Hippocampal synaptic plasticity during the pathological process of depression has received increasing attention. Hippocampal neuron atrophy and the reduction in synaptic density induced by chronic stress are important pathological mechanisms of depression. Electroacupuncture (EA) exerts beneficial effects on depression, but the mechanism is unclear. This study explored the effect of EA on synaptic plasticity and the potential mechanism. Methods Forty-eight SD rats were randomly divided into the control, chronic unpredictable mild stress (CUMS), EA, and fluoxetine (FLX) groups, and each group consisted of 12 rats. The sucrose preference test, open field test, and forced swimming test were used for the evaluation of depression-like behaviour, and Golgi and Nissl staining were used for the assessment of synaptic plasticity. Western blotting and immunofluorescence were conducted to detect proteins related to synaptic plasticity and to determine their effects on signalling pathways. Results We found that CUMS led to depression-like behaviours, including a reduced preference for sucrose, a prolonged immobility time, and reduced exploration activity. The dendritic spine densities and neuron numbers and the protein levels of MAP-2, PSD-95, and SYN were decreased in the hippocampi of rats with CUMS-induced depression, and these trends were reversed by EA. The molecular mechanism regulating this plasticity may involve the GluN2B/CaMKII/CREB signalling pathway. Conclusion These results suggest that EA can improve depression-like behaviour and hippocampal plasticity induced by CUMS, and the mechanism may be related to the GluN2B/CaMKII/CREB pathway.
Highlights
Depression is a common serious mental disease that mainly manifests as a depressed mood, declining interests, a lack of pleasure, serious insomnia, stupor and other somatic symptoms, and even suicide [1, 2]. e depression prevalence rate continues to increase, and the disease poses substantial social and economic burdens
All animals were housed under controlled temperature (23 ± 1°C) and light (12 h light/dark cycle) conditions and were adaptively fed for one week before the formal experiment. e experimental animals were randomly divided into 4 groups (12 rats in each group): the control, CUMS, EA, and fluoxetine (FLX) groups. e rats in the control group were fed normally without any intervention, and those in the CUMS, EA, and FLX groups were exposed to chronic unpredictable mild stress for 21 days and subjected to behavioural tests
We evaluated the locomotor activity of the rats via the open-field test (OFT). e OFT apparatus consisted of a 100 cm × 100 cm × 50 cm plastic board, and the floor was divided into 25 equal squares. e rats were placed at the centre of the device and allowed to freely explore the platform for 5 min. e numbers of crossings and rearings were recorded using SuperMaze 2.0 (Shanghai Xin-ruan Information Technology Co., China). e number of times the rats passed through the bottom surface was counted as the Sucrose preference test Open field test Forced swim test 21 days Figure 1: Experimental procedures
Summary
Hippocampal synaptic plasticity during the pathological process of depression has received increasing attention. Hippocampal neuron atrophy and the reduction in synaptic density induced by chronic stress are important pathological mechanisms of depression. Is study explored the effect of EA on synaptic plasticity and the potential mechanism. E sucrose preference test, open field test, and forced swimming test were used for the evaluation of depression-like behaviour, and Golgi and Nissl staining were used for the assessment of synaptic plasticity. Western blotting and immunofluorescence were conducted to detect proteins related to synaptic plasticity and to determine their effects on signalling pathways. We found that CUMS led to depression-like behaviours, including a reduced preference for sucrose, a prolonged immobility time, and reduced exploration activity. E molecular mechanism regulating this plasticity may involve the GluN2B/CaMKII/CREB signalling pathway. Ese results suggest that EA can improve depression-like behaviour and hippocampal plasticity induced by CUMS, and the mechanism may be related to the GluN2B/CaMKII/CREB pathway Conclusion. ese results suggest that EA can improve depression-like behaviour and hippocampal plasticity induced by CUMS, and the mechanism may be related to the GluN2B/CaMKII/CREB pathway
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