An excitatory synapse hypothesis of depression.

Abstract:

: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.

journal_name

Trends Neurosci

journal_title

Trends in neurosciences

authors

Thompson SM,Kallarackal AJ,Kvarta MD,Van Dyke AM,LeGates TA,Cai X

doi

10.1016/j.tins.2015.03.003

subject

Has Abstract

pub_date

2015-05-01 00:00:00

pages

279-94

issue

5

eissn

0166-2236

issn

1878-108X

pii

S0166-2236(15)00062-4

journal_volume

38

pub_type

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