ArticleMolecular psychiatry2018
Ant1 mutant mice bridge the mitochondrial and serotonergic dysfunctions in bipolar disorder.
Article in Molecular psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 42 citations in OpenAlex.
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- Genome-wide association study of delay discounting in Heterogenous Stock rats.bioRxiv : the preprint server for biology · 2023Article
- Mitochondria dysfunction and bipolar disorder: From pathology to therapy.IBRO neuroscience reports · 2023Article
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- IntelliCage: the development and perspectives of a mouse- and user-friendly automated behavioral test system.Frontiers in behavioral neuroscience · 2023Review
- A Perspective on the Potential Involvement of Impaired Proteostasis in Neuropsychiatric Disorders.Biological psychiatry · 2022Review
- Inhibition of aberrant Hif1α activation delays intervertebral disc degeneration in adult mice.Bone research · 2022Article
- Bipolar Disorder: From Pathophysiology to Treatment.Juntendo Iji zasshi = Juntendo medical journal · 2022Review
- Functional and behavioral effects of de novo mutations in calcium-related genes in patients with bipolar disorder.Human molecular genetics · 2021Article
- Mitochondria and early-life adversity.Mitochondrion · 2021Article
- Targeting Mitochondrial Dysfunction for Bipolar Disorder.Current topics in behavioral neurosciences · 2021Review
- Unbiased PCR-free spatio-temporal mapping of the mtDNA mutation spectrum reveals brain region-specific responses to replication instability.BMC biology · 2020Article
- Reply to "Correspondence to Ant1 mutant mice bridge the mitochondrial and serotonergic dysfunctions in bipolar disorder".Molecular psychiatry · 2020Article
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9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although mitochondrial and serotonergic dysfunctions have been implicated in the etiology of bipolar disorder (BD), the relationship between these unrelated pathways has not been elucidated. A family of BD and chronic progressive external ophthalmoplegia (CPEO) caused by a mutation of the mitochondrial adenine nucleotide translocator 1 (ANT1, SLC25A4) implicated that ANT1 mutations confer a risk of BD. Here, we sequenced ANT1 in 324 probands of NIMH bipolar disorder pedigrees and identified two BD patients carrying heterozygous loss-of-function mutations. Behavioral analysis of brain specific Ant1 heterozygous conditional knockout (cKO) mice using lntelliCage showed a selective diminution in delay discounting. Delay discounting is the choice of smaller but immediate reward than larger but delayed reward and an index of impulsivity. Diminution of delay discounting suggests an increase in serotonergic activity. This finding was replicated by a 5-choice serial reaction time test. An anatomical screen showed accumulation of COX (cytochrome c oxidase) negative cells in dorsal raphe. Dorsal raphe neurons in the heterozygous cKO showed hyperexcitability, along with enhanced serotonin turnover in the nucleus accumbens and upregulation of Maob in dorsal raphe. These findings altogether suggest that mitochondrial dysfunction as the genetic risk of BD may cause vulnerability to BD by altering serotonergic neurotransmission.
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