Effect of desipramine and fluoxetine on energy metabolism of cerebral mitochondria

Villa, R. F.; Ferrari, Francesca; Gorini, A.; Brunello, Nicoletta; Tascedda, Fabio

doi:10.1016/j.neuroscience.2016.05.051

Cited by 43 publications

(48 citation statements)

References 52 publications

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“…), and the antidepressant drugs Desipramine and Fluoxetine (Villa et al . , ): the treatments lead to adjustments in the neuronal energetic state, in relation to the energy requirements of pre‐ and post‐synaptic compartments after drug administrations.…”

Section: Discussionmentioning

confidence: 99%

“…This procedure allows to preserve not only metabolites, but also the catalytic activity of enzymes, permitting the subfractionation of the cerebral tissue, as previously reported (Villa et al . , , , ; Battino et al . ).…”

Section: Methodsmentioning

confidence: 99%

“…Moreover, (iii) enzyme activities may be the direct molecular targets of drugs (Villa and Gorini ; Villa et al . , , ; Moretti et al . ).…”

mentioning

confidence: 99%

“…The maximal rate (V max ) of enzyme activities involved in glutamate and related amino acids metabolism were evaluated, as indicative functional parameters of the brain tissue ability to respond (i) to pathological insults and (ii) to pharmacological treatments (Villa et al 2012b;Ferrari et al 2015b). Moreover, (iii) enzyme activities may be the direct molecular targets of drugs (Villa and Gorini 1997;Villa et al 2012bVilla et al , 2016Villa et al , 2017aMoretti et al 2015a). In this regard, the evaluation of catalytic enzyme activities provides a great advantage over the assay of metabolite concentrations, because it allows to differentiate between subcellular neuronal compartments (Villa et al 1989(Villa et al , 2012b(Villa et al , 2013aVilla and Gorini 1991).…”

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confidence: 99%

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Glutamate metabolism in cerebral mitochondria after ischemia and post‐ischemic recovery during aging: relationships with brain energy metabolism

Ferrari

Gorini

Hoyer

et al. 2018

Journal of Neurochemistry

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Glutamate is involved in cerebral ischemic injury, but its role has not been completely clarified and studies are required to understand how to minimize its detrimental effects, contemporarily boosting the positive ones. In fact, glutamate is not only a neurotransmitter, but primarily a key metabolite for brain bioenergetics. Thus, we investigated the relationships between glutamate and brain energy metabolism in an in vivo model of complete cerebral ischemia of 15 min and during post-ischemic recovery after 1, 24, 48, 72, and 96 h in 1-year-old adult and 2-year-old aged rats. The maximum rates (V ) of glutamate dehydrogenase (GlDH), glutamate-oxaloacetate transaminase, and glutamate-pyruvate transaminase were assayed in somatic mitochondria (FM) and in intra-synaptic 'Light' mitochondria and intra-synaptic 'Heavy' mitochondria ones purified from cerebral cortex, distinguishing post- and pre-synaptic compartments. During ischemia, none of the enzymes were modified in adult animals. In aged ones, glutamate-oxaloacetate transaminase was increased in FM and GlDH in intra-synaptic 'Heavy' mitochondria, stimulating glutamate catabolism. During post-ischemic recovery, FM did not show modifications at both ages while, in intra-synaptic mitochondria of adult animals, glutamate catabolism was increased after 1 h of recirculation and decreased after 48 and 72 h, whereas it remained decreased up to 96 h in aged rats. These results, with those previously published about Krebs' cycle and Electron Transport Chain (Villa et al., [2013] Neurochem. Int. 63, 765-781), demonstrate that: (i) V of energy-linked enzymes are different in the various cerebral mitochondria, which (ii) respond differently to ischemia and post-ischemic recovery, also (iii) with respect to aging.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…Moreover, (iii) enzyme activities may be the direct molecular targets of drugs (Villa and Gorini ; Villa et al . , , ; Moretti et al . ).…”

mentioning

confidence: 99%

mentioning

confidence: 99%

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Glutamate metabolism in cerebral mitochondria after ischemia and post‐ischemic recovery during aging: relationships with brain energy metabolism

Ferrari

Gorini

Hoyer

et al. 2018

Journal of Neurochemistry

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“…Our findings also corroborate with previous studies from our group with mitochondria of different tissues . Similarly, Villa, Ferrari, Gorini, Brunello, and Tascedda (2016) demonstrated that chronic Fx treatment in adult male rats increases cytochrome oxidase (complex IV) activity in the cerebral cortex (Villa et al, 2016).…”

Section: Effects Of Ssri Treatment During Developmentmentioning

confidence: 99%

Serotonin transporter inhibition during neonatal period induces sex‐dependent effects on mitochondrial bioenergetics in the rat brainstem

Silva

Freitas

et al. 2018

Eur J of Neuroscience

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The serotonin reuptake is mainly regulated by the serotonin transporters (SERTs), which are abundantly found in the raphe nuclei, located in the brainstem. Previous studies have shown that dysfunction in the SERT has been associated with several disorders, including depression and cardiovascular diseases. In this manuscript, we aimed to investigate how gender and the treatment with a serotonin selective reuptake inhibitor (SSRI) could affect mitochondrial bioenergetics and oxidative stress in the brainstem of male and female rats. Fluoxetine, our chosen SSRI, was used during the neonatal period (i.e., from postnatal Day 1 to postnatal Day 21-PND1 to PND21) in both male and female animals. Thereafter, experiments were conducted in adult rats (60 days old). Our results demonstrate that, during lactation, fluoxetine treatment modulates the mitochondrial bioenergetics in a sex-dependent manner, such as improving male mitochondrial function and female antioxidant capacity.

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Antidepressant Action on Mitochondrial Dysfunction in Psychiatric Disorders

Adžić

Brkic

Bulajić³

et al. 2016

Drug Development Research

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Preclinical Research Mitochondria are cell organelles crucial to the production of cellular energy. Several lines of evidence have indicated that mitochondrial dysfunction could be related to the pathophysiology of CNS diseases including bipolar disorder, major depressive disorder, and schizophrenia. These changes include impaired energy metabolism in the brain, co-morbidity with mitochondrial diseases, the effects of psychotropics on mitochondrial function, increased mitochondrial DNA (mtDNA) deletion in the brain, and association with mtDNA polymorphisms. Additionally, psychotropic drug treatments can alter energy metabolism and may affect mitochondrial processes. This review focuses on recent findings regarding the effects of antidepressants on mitochondrial processes in psychiatric disorders. Drug Dev Res 77 : 400-406, 2016. © 2016 Wiley Periodicals, Inc.

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Effect of desipramine and fluoxetine on energy metabolism of cerebral mitochondria

Cited by 43 publications

References 52 publications

Glutamate metabolism in cerebral mitochondria after ischemia and post‐ischemic recovery during aging: relationships with brain energy metabolism

Glutamate metabolism in cerebral mitochondria after ischemia and post‐ischemic recovery during aging: relationships with brain energy metabolism

Serotonin transporter inhibition during neonatal period induces sex‐dependent effects on mitochondrial bioenergetics in the rat brainstem

Antidepressant Action on Mitochondrial Dysfunction in Psychiatric Disorders

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