SIRT2 inhibition modulate glutamate and serotonin systems in the prefrontal cortex and induces antidepressant-like action

Erburu, M.M.; Muñoz-Cobo, I.; Diaz-Perdigón, Teresa; Mellini, Paolo; Suzuki, Takayoshi; Puerta, Elena; Tordera, Rosa M.

doi:10.1016/j.neuropharm.2017.01.033

Cited by 56 publications

(44 citation statements)

References 61 publications

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“…Given that administration of classical antidepressants, such as imipramine and fluoxetine, during the last 5 days of this same 6 weeks of chronic stress session did not produce antidepressant‐like activity, pharmacological suppression of HDAC may be a more rapidly acting therapeutic strategy. As shown in Table and in support of our findings, other reports have also shown that SAHA has a rapid antidepressant action and that SAHA treatment may be effective for depressive‐like behaviors in mice that are resistant to conventional treatments …”

Section: Histone Acetylation In Neuroplasticity Stress Responses Ansupporting

confidence: 92%

“…These new data will inform efforts to develop novel strategies for new antidepressant compounds by moving beyond monoamine transporters and receptors. As described in Table , given that HDAC inhibitors and DNMT inhibitors exert antidepressant‐like actions in several rodent models, epigenetic molecules themselves may be suitable targets for treatment. Medications targeting epigenetic modifications (e.g., HDAC and DNMT inhibitors) are already in use and are proving effective for cancers and neurodegenerative disorders .…”

Section: Limitations Future Directions and Concluding Remarksmentioning

confidence: 99%

“…Erburu et al 77 Repeated administration prevents stressinduced spine loss. Repeated administration has antianhedonic effects.…”

Section: Srt2104mentioning

confidence: 99%

“…These new data will inform efforts to develop novel strategies for new antidepressant compounds by moving beyond monoamine transporters and receptors. As described in Table 1, given that HDAC inhibitors and DNMT inhibitors exert antidepressant-like actions in several rodent models, [15][16][17]66,69,[71][72][73][74][75][76][77][78][79][80]164 epigenetic molecules themselves may be suitable targets for treatment.…”

Section: Limitations Future Directions and Concluding Remarksmentioning

confidence: 99%

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Epigenetic mechanisms of major depression: Targeting neuronal plasticity

Uchida

Yamagata

Seki

et al. 2017

Psychiatry Clin Neurosci

125

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Major depressive disorder is one of the most common mental illnesses as it affects more than 350 million people globally. Major depressive disorder is etiologically complex and disabling. Genetic factors play a role in the etiology of major depression. However, identical twin studies have shown high rates of discordance, indicating non‐genetic mechanisms as well. For instance, stressful life events increase the risk of depression. Environmental stressors also induce stable changes in gene expression within the brain that may lead to maladaptive neuronal plasticity in regions implicated in disease pathogenesis. Epigenetic events alter the chromatin structure and thus modulate expression of genes that play a role in neuronal plasticity, behavioral response to stress, depressive behaviors, and response to antidepressants. Here, we review new information regarding current understanding of epigenetic events that may impact depression. In particular, we discuss the roles of histone acetylation, DNA methylation, and non‐coding RNA. These novel mechanisms of action may lead to new therapeutic strategies for treating major depression.

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Section: Histone Acetylation In Neuroplasticity Stress Responses Ansupporting

confidence: 92%

Section: Limitations Future Directions and Concluding Remarksmentioning

confidence: 99%

“…Erburu et al 77 Repeated administration prevents stressinduced spine loss. Repeated administration has antianhedonic effects.…”

Section: Srt2104mentioning

confidence: 99%

“…These new data will inform efforts to develop novel strategies for new antidepressant compounds by moving beyond monoamine transporters and receptors. As described in Table 1, given that HDAC inhibitors and DNMT inhibitors exert antidepressant-like actions in several rodent models, [15][16][17]66,69,[71][72][73][74][75][76][77][78][79][80]164 epigenetic molecules themselves may be suitable targets for treatment.…”

Section: Limitations Future Directions and Concluding Remarksmentioning

confidence: 99%

See 2 more Smart Citations

Epigenetic mechanisms of major depression: Targeting neuronal plasticity

Uchida

Yamagata

Seki

et al. 2017

Psychiatry Clin Neurosci

125

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“…Among the few transcriptional regulators upregulated are Sirt2, Elmo1, Zcchc12 , none of which have been characterized in the context of MGE function (Figure4B ii ) . Sirt2 is an established transcriptional repressor [66, 67] that may regulate the repression of several target genes in an MGE-specific manner, and Elmo1 has been previously characterized during the activity-dependent migration of CGE subtypes [21]. Finally, a recent study has predicted that the expression of Zcchc12 correlates with slower intrinsic firing among hippocampal CA1 interneurons [43].…”

Section: Resultsmentioning

confidence: 99%

NMDAR-mediated transcriptional control of gene expression during the development of medial ganglionic eminence-derived interneurons

Mahadevan

Mitra²,

Zhang

et al. 2020

Preprint

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Medial ganglionic eminence (MGE)-derived parvalbumin (PV)+, somatostatin (SST)+ and Neurogliaform (NGFC)-type cortical and hippocampal interneurons, have distinct molecular, anatomical and physiological properties. However, the molecular mechanisms regulating their diversity remain poorly understood. Here, via single-cell transcriptomics, we show that the obligate NMDA-type glutamate receptor (NMDAR) subunit gene Grin1 mediates subtype-specific transcriptional regulation of gene expression in MGE-derived interneurons, leading to altered subtype identities. Notably, MGE-specific conditional Grin1 loss results in a systemic downregulation of diverse transcriptional, synaptogenic and membrane excitability regulatory programs. These widespread gene expression abnormalities mirror aberrations that are typically associated with neurodevelopmental disorders, particularly schizophrenia.Our study hence provides a road map for the systematic examination of NMDAR signaling in interneuron subtypes, revealing potential MGE-specific genetic targets that could instruct future therapies of psychiatric disorders. 14

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Linking Depression to Epigenetics: Role of the Circadian Clock

Sato

Sassone–Corsi

2021

Circadian Clock in Brain Health and Disease

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SIRT2 inhibition modulate glutamate and serotonin systems in the prefrontal cortex and induces antidepressant-like action

Cited by 56 publications

References 61 publications

Epigenetic mechanisms of major depression: Targeting neuronal plasticity

Epigenetic mechanisms of major depression: Targeting neuronal plasticity

NMDAR-mediated transcriptional control of gene expression during the development of medial ganglionic eminence-derived interneurons

Linking Depression to Epigenetics: Role of the Circadian Clock

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