Consequences of changes in BDNF levels on serotonin neurotransmission, 5-HT transporter expression and function: Studies in adult mice hippocampus

Deltheil, Thierry; Guiard, Bruno P.; Guilloux, Jean‐Philippe; Nicolas, Lorelei; Deloménie, Claudine; Repérant, Christelle; Maître, Erwan Le; Leroux-Nicollet, Isabelle; Benmansour, Saloua; François, Clément; David, D. J.; Gardier, Alain M.

doi:10.1016/j.pbb.2007.09.018

Cited by 52 publications

(33 citation statements)

References 35 publications

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“…In this study, the authors reported that BDNF heterozygotes are less responsive to the effects of SSRI drugs, which typically increase extracellular serotonin in wild-type mice (Daws et al, 2007). In agreement with these findings, in vivo microdialysis studies demonstrate that BDNF heterozygous mice display enhanced extracellular serotonin (Deltheil et al, 2008b). BDNF heterozygotes were also found to have decreased serotonin outflow after treatment with various SSRIs, again suggesting that BDNF is involved in the action of SSRIs (Deltheil et al, 2008b).…”

Section: Brain-derived Neurotrophic Factorsupporting

confidence: 71%

“…In agreement with these findings, in vivo microdialysis studies demonstrate that BDNF heterozygous mice display enhanced extracellular serotonin (Deltheil et al, 2008b). BDNF heterozygotes were also found to have decreased serotonin outflow after treatment with various SSRIs, again suggesting that BDNF is involved in the action of SSRIs (Deltheil et al, 2008b). Investigators further showed that this impact of BDNF on 5HT function is region-specific, indicating that BDNF heterozygous mice display blunted 5HT outflow in ventral hippocampus after treatment with SSRIs (Deltheil et al, 2008a).…”

Section: Brain-derived Neurotrophic Factormentioning

confidence: 55%

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Brain-Derived Neurotrophic Factor and Neuropsychiatric Disorders

Autry

Monteggia²

2012

Pharmacol Rev

1,157

764

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Section: Brain-derived Neurotrophic Factorsupporting

confidence: 71%

Section: Brain-derived Neurotrophic Factormentioning

confidence: 55%

Brain-Derived Neurotrophic Factor and Neuropsychiatric Disorders

Autry

Monteggia²

2012

Pharmacol Rev

1,157

764

View full text Add to dashboard Cite

“…It was found that BDNF increases the activity of brain monoaminergic systems in rats [Siuciak et al, 1996]. Furthermore, BDNF plays important roles in the proliferation of neurotransmitter systems, including dopamine and serotonin [Berton et al, 2006;Deltheil et al, 2008]. Based on the shown protective effects of BDNF on the neurotoxindamaged serotonergic axons, it has been suggested that BDNF may have a physiologic role in regulating the survival of serotonergic neurons in the adult brain [Mamounas et al, 1995].…”

Section: Introductionmentioning

confidence: 99%

Brain‐derived neurotrophic factor gene Val66Met polymorphism and cognitive function in obsessive–compulsive disorder

Tükel

Gürvit

Özata

et al. 2012

American J of Med Genetics Pt B

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In the present study, we have tested the hypothesis that brain-derived neurotrophic factor (BDNF) gene Val66Met polymorphism is associated with obsessive-compulsive disorder (OCD) and also investigated the association between the BDNF Val66Met polymorphism and the performance on tests measuring executive functions in a sample of patients with OCD. A total of 100 patients diagnosed with OCD according to DSM-IV criteria and 110 control subjects were included in this study. Single nucleotide polymorphism (G/A) leading to Val to Met substitution at codon 66 in BDNF was screened in the DNA samples of all participants. The genotype frequencies of BDNF Val66Met polymorphism were compared in OCD patients and healthy controls. The four subgroups of OCD and healthy control subjects, determined according to being Val homozygous or carrying a Met allele, were also compared according to their performance in a battery of neuropsychological tests of executive functions and verbal memory. There was no significant difference for the allele and genotype distributions of BDNF Val66Met polymorphism between the OCD and healthy control groups. Compared to the other three subgroups, OCD-Met carriers were slower on Trail-Making Test part A (TMT A), part B (TMT B) score and its speed-corrected score (TMT B-A). OCD-Met carriers had also poor performance on verbal fluency tasks and several CVLT measures compared only to the healthy control-Met carriers. These results demonstrate that the BDNF Val66Met polymorphism does not appear to be a risk factor for OCD. However, the presence of a BDNF Met allele, which is a known attenuator of BDNF activity, may be associated with a poorer executive functioning in OCD.

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“…Indeed, both acute (Kozisek et al, 2008) and chronic (Deltheil et al, 2008b) administration of selective serotonin reuptake inhibitors (SSRIs) increased both mRNA and protein expression of BDNF in this brain region (Deltheil et al, 2008a). Conversely, 5-HT depletion in the hippocampus decreased mRNA expression of BDNF in rats and, in addition, caused increased anxiety-like behavior and learning impairments (Zhou et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Brain‐derived neurotrophic factor expression is increased in the hippocampus of 5‐HT_2C receptor knockout mice

et al. 2011

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Several studies have suggested a close interaction between serotonin (5-HT) and BDNF; however, little is known of the specific relationship between BDNF and the 5-HT(2C) receptor. Therefore, in this study we investigated BDNF expression in 5-HT(2C) receptor knockout mice (5-HT(2C) KO). We also assessed functional consequences of any changes in BDNF using a behavioral test battery. Western blot analysis demonstrated a significant 2.2-fold increase in the expression of the mature form of BDNF in 5-HT(2C) KO mice when compared with wild-type controls (WT) in the hippocampus (P = 0.008), but not frontal cortex or striatum. No differences in the expression of the pro-BDNF isoform were found, and the ratio of mature/pro BDNF was significantly increased in 5-HT(2C) KO (P = 0.003). BDNF mRNA expression in the hippocampus was not different between the genotypes. Hence, increased mature BDNF levels in 5-HT(2C) KO hippocampus are most likely due to increased extracellular cleavage rates of pro-BDNF to its mature form. Protein expression of the BDNF receptor, tropomycin-related receptor B (TrkB), was also unchanged in the hippocampus, frontal cortex and striatum. With repeated training in a 10-day win-shift radial arm maze task, 5-HT(2C) KO and WT showed similar decreases of the number of working memory and reference memory errors. In addition, no genotype specific differences were observed for passive or active avoidance learning. 5-HT(2C) KO showed modest locomotor hyperactivity but no differences in tests for anxiety, sensorimotor gating, or depressive-like behaviors; however, in the tail suspension test 5-HT(2C) KO showed significantly reduced climbing (P < 0.05). In conclusion, loss of 5-HT(2C) receptor expression leads to a marked and selective increase in levels of the mature form of BDNF in the hippocampus. Despite this marked increase, 5-HT(2C) KO show only subtle behavioral changes.

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Consequences of changes in BDNF levels on serotonin neurotransmission, 5-HT transporter expression and function: Studies in adult mice hippocampus

Cited by 52 publications

References 35 publications

Brain-Derived Neurotrophic Factor and Neuropsychiatric Disorders

Brain-Derived Neurotrophic Factor and Neuropsychiatric Disorders

Brain‐derived neurotrophic factor gene Val66Met polymorphism and cognitive function in obsessive–compulsive disorder

Brain‐derived neurotrophic factor expression is increased in the hippocampus of 5‐HT_2C receptor knockout mice

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Consequences of changes in BDNF levels on serotonin neurotransmission, 5-HT transporter expression and function: Studies in adult mice hippocampus

Cited by 52 publications

References 35 publications

Brain-Derived Neurotrophic Factor and Neuropsychiatric Disorders

Brain-Derived Neurotrophic Factor and Neuropsychiatric Disorders

Brain‐derived neurotrophic factor gene Val66Met polymorphism and cognitive function in obsessive–compulsive disorder

Brain‐derived neurotrophic factor expression is increased in the hippocampus of 5‐HT2C receptor knockout mice

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Product

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Brain‐derived neurotrophic factor expression is increased in the hippocampus of 5‐HT_2C receptor knockout mice