期刊
TRENDS IN NEUROSCIENCES
卷 38, 期 5, 页码 279-294出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2015.03.003
关键词
glutamate; stress; ketamine; reward; hippocampus; nucleus accumbens
资金
- [R01 MH086828]
- [T32 GM008181]
- [T32 NS063391]
- [T32 NS007375]
Depression is a common cause of mortality and morbidity, but the biological bases of the deficits in emotional and cognitive processing remain incompletely understood. Current antidepressant therapies are effective in only some patients and act slowly. Here, we propose an excitatory synapse, hypothesis of depression in which chronic stress and genetic susceptibility cause changes in the strength of subsets of glutamatergic synapses at multiple locations, including the prefrontal cortex (PFC), hippocampus, and nucleus accumbens (NAc), leading to a dysfunction of corticomesolimbic reward circuitry that underlies many of the symptoms of depression. This hypothesis accounts for current depression treatments and suggests an updated framework for the development of better therapeutic compounds.
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