Synaptic activity-dependent modulation of mitochondrial gene expression in the rat hippocampus

Williams, Joanna M.; Thompson, Vida L.; Mason-Parker, Sara E.; Abraham, Wickliffe C.; Tate, Warren P.

doi:10.1016/s0169-328x(98)00165-x

Cited by 54 publications

(39 citation statements)

References 34 publications

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“…Additionally, ESRRA has a well-established role in mitochondrial biogenesis, and several papers have identified a role for mitochondrial functioning in neuronal plasticity. For instance, mitochondria are abundant in the synapse and affect several key processes, including neurotransmitter synthesis and release, calcium buffering, and ATP synthesis (37,38), and the expression of mitochondrial genes is induced by synaptic activity in rodents (39). Furthermore, disruption of metabolic pathways in the mitochondria has been identified in synaptic vesicles prepared from the anterior cingulate cortex of mice with high anxiety (40), a trait frequently observed in ED patients (41).…”

Section: Discussionmentioning

confidence: 99%

Eating disorder predisposition is associated with ESRRA and HDAC4 mutations

Cui¹,

Moore²,

Ashimi³

et al. 2013

J. Clin. Invest.

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Anorexia nervosa and bulimia nervosa are common and severe eating disorders (EDs) of unknown etiology. Although genetic factors have been implicated in the psychopathology of EDs, a clear biological pathway has not been delineated. DNA from two large families affected by EDs was collected, and mutations segregating with illness were identified by whole-genome sequencing following linkage mapping or by whole-exome sequencing. In the first family, analysis of twenty members across three generations identified a rare missense mutation in the estrogen-related receptor α (ESRRA) gene that segregated with illness. In the second family, analysis of eight members across four generations identified a missense mutation in the histone deacetylase 4 (HDAC4) gene that segregated with illness. ESRRA and HDAC4 were determined to interact both in vitro in HeLa cells and in vivo in mouse cortex. Transcriptional analysis revealed that HDAC4 potently represses the expression of known ESRRA-induced target genes. Biochemical analysis of candidate mutations revealed that the identified ESRRA mutation decreased its transcriptional activity, while the HDAC4 mutation increased transcriptional repression of ESRRA. Our findings suggest that mutations that result in decreased ESRRA activity increase the risk of developing EDs.

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Section: Discussionmentioning

confidence: 99%

Eating disorder predisposition is associated with ESRRA and HDAC4 mutations

Cui¹,

Moore²,

Ashimi³

et al. 2013

J. Clin. Invest.

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“…Additionally, it is intriguing that the CA3b sector of pilocarpine-treated rats displayed highly specific changes due to altered activity of enzymes involved in mitochondrial oxidative phosphorylation, leading to a decrease in maximal rates of hippocampal slice respiration and partial mitochondrial membrane depolarization [38]. In contrast, upregulation of enzymes containing mitochondrial-encoded subunits was observed in the presence of increased neuronal activity in normal hippocampal tissue [39], so that data showing the decreased enzymatic activity in the mitochondria of pilocarpine-treated rats [38] may be explained by the lower level of pyramidal cell activation that we observed by different techniques [17,34].…”

Section: Histological Evidence For Ischemic Damage In the Ca3 Regionmentioning

confidence: 99%

Ischemic–hypoxic mechanisms leading to hippocampal dysfunction as a consequence of status epilepticus

Lucchi

Vinet

Meletti

et al. 2015

Epilepsy & Behavior

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“…19 Indeed, events in learning and memory processes, such as long-term potentiation (LTP), have been associated with changes in mitochondria. [20][21][22] Other studies suggest that mitochondria work as mediators of some of the effects of glutamate and brain-derived neurotrophic factor (BDNF) on synaptic plasticity. BDNF is known to promote synaptic plasticity, partly because it enhances mitochondrial energy production 23 and increases mitochondrial respiratory coupling at complex I.…”

Section: Mitochondria: the Crucial Signalingmentioning

confidence: 99%

Mitochondria and the central nervous system: searching for a pathophysiological basis of psychiatric disorders

Streck

Gonçalves

Furlanetto

et al. 2014

Rev. Bras. Psiquiatr.

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Introduction: Mitochondrial dysfunction has been postulated to participate in the development of many neuropsychiatric disorders, but there is no consensus as to its role. The aim of this paper is to review recent studies and to outline the current understanding of the association between mitochondrial dysfunction and psychiatric disorders. Methodology: We reviewed articles that evaluated mitochondrial dysfunction and psychiatric disorders, with a particular focus on depression, bipolar disorder, anxiety disorders, obsessivecompulsive disorder, and autism spectrum disorder, and the association between mitochondrial dysfunction and development of these disorders. Results: Evidence suggests that alterations in mitochondrial morphology, brain energy metabolism, and mitochondrial enzyme activity may be involved in the pathophysiology of different neuropsychiatric disorders, given their key role in energy metabolism in the cell. Conclusions: Understanding the interactions between mitochondrial dysfunction and development of psychiatric disorders may help establish more effective therapeutic strategies for these disorders and thus lead to better outcomes for affected subjects.

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Synaptic activity-dependent modulation of mitochondrial gene expression in the rat hippocampus

Cited by 54 publications

References 34 publications

Eating disorder predisposition is associated with ESRRA and HDAC4 mutations

Eating disorder predisposition is associated with ESRRA and HDAC4 mutations

Ischemic–hypoxic mechanisms leading to hippocampal dysfunction as a consequence of status epilepticus

Mitochondria and the central nervous system: searching for a pathophysiological basis of psychiatric disorders

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