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Depression-like episodes in mice harboring mtDNA deletions in paraventricular thalamus.

Abstract：

:Depression is a common debilitating human disease whose etiology has defied decades of research. A critical bottleneck is the difficulty in modeling depressive episodes in animals. Here, we show that a transgenic mouse with chronic forebrain expression of a dominant negative mutant of Polg1, a mitochondrial DNA (mtDNA) polymerase, exhibits lethargic behavioral changes, which are associated with emotional, vegetative and psychomotor disturbances, and response to antidepression drug treatment. The results suggested a symptomatic similarity between the lethargic behavioral change that was recurrently and spontaneously experienced by the mutant mice and major depressive episode as defined by DSM-5. A comprehensive screen of mutant brain revealed a hotspot for mtDNA deletions and mitochondrial dysfunction in the paraventricular thalamic nucleus (PVT) with similar defects observed in postmortem brains of patients with mitochondrial disease with mood symptoms. Remarkably, the genetic inhibition of PVT synaptic output by Cre-loxP-dependent expression of tetanus toxin triggered de novo depression-like episodes. These findings identify a novel preclinical mouse model and brain area for major depressive episodes with mitochondrial dysfunction as its cellular mechanism.

journal_name

Mol Psychiatry

journal_title

Molecular psychiatry

authors

Kasahara T,Takata A,Kato TM,Kubota-Sakashita M,Sawada T,Kakita A,Mizukami H,Kaneda D,Ozawa K,Kato T

doi

10.1038/mp.2015.156

subject

Has Abstract

pub_date

2016-01-01 00:00:00

pages

39-48

issue

1

eissn

1359-4184

issn

1476-5578

pii

mp2015156

journal_volume

21

pub_type

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