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• W2022082745 abstract "Chronic stress is a strong diathesis for depression in humans and is used to generate animal models of depression. It commonly leads to several major symptoms of depression, including dysregulated feeding behaviour, anhedonia and behavioural despair. Although hypotheses defining the neural pathophysiology of depression have been proposed, the critical synaptic adaptations in key brain circuits that mediate stress-induced depressive symptoms remain poorly understood. Here we show that chronic stress in mice decreases the strength of excitatory synapses on D1 dopamine receptor-expressing nucleus accumbens medium spiny neurons owing to activation of the melanocortin 4 receptor. Stress-elicited increases in behavioural measurements of anhedonia, but not increases in measurements of behavioural despair, are prevented by blocking these melanocortin 4 receptor-mediated synaptic changes in vivo. These results establish that stress-elicited anhedonia requires a neuropeptide-triggered, cell-type-specific synaptic adaptation in the nucleus accumbens and that distinct circuit adaptations mediate other major symptoms of stress-elicited depression. Stress-induced behavioural measures of anhedonia in adult mice, but not measures of behavioural despair, required a decrease in the strength of excitatory synapses on D1 dopamine receptor-expressing nucleus accumbens medium spiny neurons owing to activation of melanocortin 4 receptors. Chronic stress is known to lead to symptoms of depression, such as an inability to feel pleasure (anhedonia), abnormal eating habits and behavioural despair, but the synaptic adaptations involved in the various symptoms are not well understood. This study in mice shows that stress decreases the strength of excitatory synapses onto D1 dopamine-receptor-expressing neurons in the nucleus accumbens, part of the brain associated with pleasure and reward-seeking behaviour, through activation of melanocortin 4 receptors. Blocking these receptors prevents the effects of stress on feeding and cocaine-reward responses, but not behavioural despair. These results provide evidence of a dissociation between the neural circuits that mediate different symptoms of depression, suggesting that it should be possible to develop therapies targeting specific behaviours." @default.
• W2022082745 created "2016-06-24" @default.
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• W2022082745 date "2012-07-01" @default.
• W2022082745 modified "2023-10-04" @default.
• W2022082745 title "Anhedonia requires MC4R-mediated synaptic adaptations in nucleus accumbens" @default.
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• W2022082745 doi "https://doi.org/10.1038/nature11160" @default.
• W2022082745 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3397405" @default.
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