Chronic Fluoxetine Treatment Induces Brain Region-Specific Upregulation of Genes Associated with BDNF-Induced Long-Term Potentiation

Alme, Maria Nordheim; Wibrand, Karin; Dagestad, Grethe; Bramham, Clive R.

doi:10.1155/2007/26496

Cited by 83 publications

(75 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These results are in line with the findings from animal models in which NRN1 is shown as an interesting new player in depression. In this regard, knockdown of NRN1 mice models in the hippocampus produced depressive-like behaviours (Son et al 2012), whereas electroconvulsive therapy and antidepressant treatment produced changes in Neuritin levels (Alme et al 2007;Dyrvig et al 2014). In all, these results suggest the role of NRN1 in modulating depressive symptomatology and highlights this gene as a potentially interesting new target for antidepressant treatment.…”

Section: Discussionmentioning

confidence: 76%

“…Second, electroconvulsive therapy, one of the most robust gene inducer among all antidepressant treatments (Segi-Nishida 2011), induces changes in both NRN1 and BDNF expression (Dyrvig M et al 2014;Park HG et al 2014). Third, fluoxetine increases the level of NRN1 and BDNF specifically in the prefrontal cortex, hippocampus and dentate gyrus (Alme et al 2007), which suggest that antidepressant treatment promotes gene expression responses linked to NTFs signaling and synaptic plasticity.…”

Section: Introductionmentioning

confidence: 98%

See 1 more Smart Citation

Role of neurotrophins in depressive symptoms and executive function: Association analysis of NRN1 gene and its interaction with BDNF gene in a non-clinical sample

Prats

Arias

Ortet

et al. 2017

Journal of Affective Disorders

View full text Add to dashboard Cite

word count: 248Word count: Tables: 3 Figures: 2 Number of references: ABSTRACT Background: Neuritin-1 (NRN1) is a neurotrophic factor involved in synaptic plasticity that has been associated with schizophrenia, depressive disorders and cognitive performance. Considering that the study of genotype-phenotype relationship in healthy individuals is a useful framework to investigate the etiology of brain dysfunctions that underlie mental disorders, we aimed to study in a general population sample, whether NRN1 gene variability is contributing to: i) the psychopathological profile, ii) the executive function performance. We also aimed to test whether these associations are modulated by BDNF gene.

show abstract

Section: Discussionmentioning

confidence: 76%

Section: Introductionmentioning

confidence: 98%

Role of neurotrophins in depressive symptoms and executive function: Association analysis of NRN1 gene and its interaction with BDNF gene in a non-clinical sample

Prats

Arias

Ortet

et al. 2017

Journal of Affective Disorders

View full text Add to dashboard Cite

show abstract

“…Neuritin has been implicated in the actions of BDNF (9,18), which is up-regulated in the hippocampus by antidepressant treatment and is sufficient to produce antidepressant behavioral responses (19,20). Moreover, chronic antidepressant treatment has been shown to increase neuritin expression in rat brain (21). The current study was conducted to test the hypothesis that neuritin is a critical downstream mediator of antidepressant/BDNF-mediated plasticity and, conversely, that loss of neuritin could contribute to depressive symptoms caused by stress exposure.…”

mentioning

confidence: 99%

Neuritin produces antidepressant actions and blocks the neuronal and behavioral deficits caused by chronic stress

Son

Banasr

Choi³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Decreased neuronal dendrite branching and plasticity of the hippocampus, a limbic structure implicated in mood disorders, is thought to contribute to the symptoms of depression. However, the mechanisms underlying this effect, as well as the actions of antidepressant treatment, remain poorly characterized. Here, we show that hippocampal expression of neuritin, an activity-dependent gene that regulates neuronal plasticity, is decreased by chronic unpredictable stress (CUS) and that antidepressant treatment reverses this effect. We also show that viral-mediated expression of neuritin in the hippocampus produces antidepressant actions and prevents the atrophy of dendrites and spines, as well as depressive and anxiety behaviors caused by CUS. Conversely, neuritin knockdown produces depressive-like behaviors, similar to CUS exposure. The ability of neuritin to increase neuroplasticity is confirmed in models of learning and memory. Our results reveal a unique action of neuritin in models of stress and depression, and demonstrate a role for neuroplasticity in antidepressant treatment response and related behaviors.is a devastating and recurrent illness affecting up to 17% of the population, resulting in personal disability, increased rates of suicide, and socioeconomic loss (1). Moreover, currently available antidepressants are only effective in approximately one-third of patients with MDD and in up to two-thirds after multiple trials, and they take weeks to months to produce a response (2, 3). In addition, the mechanisms underlying the therapeutic actions of antidepressants are poorly understood. New targets beyond monoamine signaling are now emerging in both preclinical and clinical reports of MDD (4, 5). These studies have focused on key limbic brain structures, including the hippocampus, that are significantly altered by chronic stress and depression and that are known to regulate mood, anxiety, and cognition (6, 7). Hippocampal synaptic plasticity has received much attention in recent years because human imaging and rodent studies demonstrate that stress and depression are associated with decreased hippocampal volume and atrophy of neurons (6,8).Neuritin, also known as candidate plasticity gene 15 (CPG15), encodes a small, extracellular GPI-anchored protein critical for dendritic outgrowth, maturation, and axonal regeneration (9-13). Neuritin expression in the hippocampus is induced by neuronal activity following chemical-or electrical-induced seizures (9, 14, 15), ischemia (16), and exercise (5, 17). Neuritin has been implicated in the actions of BDNF (9, 18), which is up-regulated in the hippocampus by antidepressant treatment and is sufficient to produce antidepressant behavioral responses (19,20). Moreover, chronic antidepressant treatment has been shown to increase neuritin expression in rat brain (21). The current study was conducted to test the hypothesis that neuritin is a critical downstream mediator of antidepressant/BDNF-mediated plasticity and, conversely, that loss of neuritin could contribute to depre...

show abstract

“…Riluzole, is an inhibitor of tetradotoxin-sensitive voltage-gated sodium channels, with antiglutamatergic profile, and the only established disease-modifying treatment for amyotrophic lateral sclerosis [56]. Fluoxetine is a selective serotonin reuptake inhibitor that has been suggested to have neuroprotective properties by supression of microglia activation, and NF-κB (a family of transcription factors with an essential role in inflammation and innate immunity) activity, and enhancement of the production of the brain-derived neurotrophic factor in animal models [57][58][59]. A 4-arm phase II trial of amiloride, fluoxetine, and riluzole (compared with placebo) is currently in progress (NCT01910259).…”

Section: Amiloride Fluoxetine and Riluzolementioning

confidence: 99%

Therapeutic Advances and Future Prospects in Progressive Forms of Multiple Sclerosis

2016

View full text Add to dashboard Cite

Identifying effective therapies for the treatment of progressive forms of multiple sclerosis (MS) is a highly relevant priority and one of the greatest challenges for the global MS community. Better understanding of the mechanisms involved in progression of the disease, novel trial designs, drug repurposing strategies, and new models of collaboration may assist in identifying effective therapies. In this review, we discuss various therapies under study in phase II or III trials, including antioxidants (idebenone); tyrosine kinase inhibitors ( m a s i t i n i b ) ; s p h i n g o s i n e r e c e p t o r m o d u l a t o r s (siponimod); monoclonal antibodies (anti-leucine-rich repeat and immunoglobulin-like domain containing neurite outgrowth inhibitor receptor-interacting protein-1, natalizumab, ocrelizumab, intrathecal rituximab); hematopoetic stem cell therapy; statins and other possible neuroprotective agents (amiloride, riluzole, fluoxetine, oxcarbazepine); lithium; phosphodiesterase inhibitors (ibudilast); hormone-based therapies (adrenocorticotrophic hormone and erythropoietin); T-cell receptor peptide vaccine (NeuroVax); autologous T-cell immunotherapy (Tcelna); MIS416 (a microparticulate immune response modifier); dopamine antagonists (domperidone); and nutritional supplements, including lipoic acid, biotin, and sunphenon epigallocatechin-3-gallate (green tea extract). Given ongoing and planned clinical trial initiatives, and the largest ever focus of the global research community on progressive MS, future prospects for developing targeted therapeutics aimed at reducing disability in progressive forms of MS appear promising.

show abstract

Chronic Fluoxetine Treatment Induces Brain Region-Specific Upregulation of Genes Associated with BDNF-Induced Long-Term Potentiation

Cited by 83 publications

References 61 publications

Role of neurotrophins in depressive symptoms and executive function: Association analysis of NRN1 gene and its interaction with BDNF gene in a non-clinical sample

Role of neurotrophins in depressive symptoms and executive function: Association analysis of NRN1 gene and its interaction with BDNF gene in a non-clinical sample

Neuritin produces antidepressant actions and blocks the neuronal and behavioral deficits caused by chronic stress

Therapeutic Advances and Future Prospects in Progressive Forms of Multiple Sclerosis

Contact Info

Product

Resources

About