BDNF controls dopamine D3 receptor expression and triggers behavioural sensitization

Guillin, Olivier; Díaz, Jorge; Carroll, Patrick; Griffon, Nathalie; Schwartz, Jean‐Charles; Sokoloff, Pierre

doi:10.1038/35075076

Cited by 521 publications

(369 citation statements)

References 29 publications

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“…76,77 We found that administration of antipsychotic drugs, such as haloperidol and risperidone, decreased levels of BDNF in the frontal and occipital cortex and hippocampus, whereas only haloperidol, which mainly acts on the dopamine(DA)-D 2 and D 3 receptors, significantly reduced the number of TrkBimmunoreactive neurons in the hippocampus, substantia nigra and ventral tegmental area. 78 These studies support the hypothesis that antipsychotic drugs exert their effect, at least in part, by modifying the synthesis and distribution of BDNF in selected brain regions.…”

Section: Bdnf and Animal Models Of Schizophreniasupporting

confidence: 60%

BDNF in schizophrenia, depression and corresponding animal models

2005

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Understanding the etiology and pathogenesis schizophrenia and depression is a major challenge facing psychiatry. One hypothesis is that these disorders are secondary to a malfunction of neurotrophic factors. Inappropriate neurotrophic support during brain development could lead to structural disorganisation in which neuronal networks are established in a nonoptimal manner. Inadequate neurotrophic support in adult individuals could ultimately be an underlying mechanism leading to decreased capacity of brain to adaptive changes and increased vulnerability to neurotoxic damage. Brain-derived neurotrophic factor (BDNF) is a mediator involved in neuronal survival and plasticity of dopaminergic, cholinergic, and serotonergic neurons in the central nervous system (CNS). In this review, we summarize findings regarding altered BDNF in schizophrenia and depression and animal models, as well as the effects of antipsychotic and antidepressive treatments on the expression of BDNF. Molecular Psychiatry (2005) 10, 345-352.

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Section: Bdnf and Animal Models Of Schizophreniasupporting

confidence: 60%

BDNF in schizophrenia, depression and corresponding animal models

2005

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“…(2016) have shown how the parents’ serotonin transporter genotype moderates the association between child noncompliance and parental negativity. We chose to focus on the brain‐derived neurotrophic factor (BDNF), which has been associated with both the serotonergic (Eaton, Staley, Globus, & Whittemore, 1995; Mamounas, Blue, Siuciak, & Altar, 1995) and dopaminergic systems (Guillin et al., 2001; Küppers & Beyer, 2001). …”

Section: Introductionmentioning

confidence: 99%

Parental brain‐derived neurotrophic factor genotype, child prosociality, and their interaction as predictors of parents’ warmth

Avinun

Knafo‐Noam

2017

Brain and Behavior

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BackgroundParental warmth has been associated with various child behaviors, from effortful control to callous‐unemotional traits. Factors that have been shown to affect parental warmth include heritability and child behavior. However, there is limited knowledge about which specific genes are involved, how they interact with child behavior, how they affect differential parenting, and how they affect fathers. We examined what affects paternal and maternal warmth by focusing on the child's prosocial behavior and parents’ genotype, specifically a Valine to Methionine substitution at codon 66 in the brain‐derived neurotrophic factor (BDNF) gene.MethodsData was available from a sample of 6.5 year‐old twins, consisting of 369 mothers and 663 children and 255 fathers and 458 children. Self‐reports were used to assess mothers’ and fathers’ warmth. Child prosociality was assessed with the other‐parent report and experimental assessments.ResultsMothers’ warmth was not affected by their BDNF genotype, neither as a main effect nor in an interaction with child prosociality. Fathers with the Met allele scored higher on warmth. Additionally, there was a significant interaction between fathers’ BDNF genotype and child prosociality. For fathers with the Met allele there was a positive association between warmth and child prosociality. Conversely, for fathers with the Val/Val genotype there was no association between warmth and child prosociality. Results were repeated longitudinally in a subsample with data on age 8–9 years. A direct within family analysis showed that fathers with the Met allele were more likely than Val/Val carriers to exhibit differential parenting toward twins who differed in their prosocial behavior. The same pattern of findings was found with mother‐rated and experimentally assessed prosociality.ConclusionsThese results shed light on the genetic and environmental underpinnings of paternal behavior and differential parenting.

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“…8,9 BDNF has regulatory effects on multiple neurotransmitter systems, including serotonin 10 and dopamine, 11 and maybe involved in the etiology of stress-related disorders, such as depression and PTSD. Chronic administration of antidepressants, including selective serotonin reuptake inhibitors, increases BDNF expression in the hippocampus.…”

Section: Introductionmentioning

confidence: 99%

No association between the brain-derived neurotrophic factor gene and panic disorder in Japanese population

et al. 2009

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Panic disorder (PD) is a severe and chronic psychiatric disorder, with significant genetic components in the etiology. Brain-derived neurotrophic factor (BDNF) gene, which has regulatory effects on neurotransmitter systems such as serotonin and dopamine, is a candidate for susceptibility locus of PD. This study investigated three single-nucleotide polymorphisms (SNPs) of BDNF (rs6265 (Val66Met), rs11030104 and rs7103411) in Japanese patients with PD and controls. No significant association was observed between the three SNPs and PD. No association of the Val66Met was consistent with two small studies in Japanese and Chinese populations. We therefore conclude that the BDNF polymorphism may not play a major role in PD in the East Asian populations. Keywords: brain-derived neurotrophic factor; genetic association; Japanese population; panic disorder; Val66Met polymorphism INTRODUCTION Panic disorder (PD) is an anxiety disorder characterized by panic attacks and anticipatory anxiety, with a lifetime prevalence of 1-3% and a female/male ratio of 2:1. 1 PD frequently takes a chronic course, with many remissions and relapses, occasionally complicated by comorbidity with other psychiatric disorders, such as agoraphobia and major depression. 2 It is generally accepted that PD has genetic as well as environmental causes. A 2.6-to 20-fold relative risk in the firstdegree relatives of proband with PD compared with the general population suggests a familial component in this disorder. 3,4 Twin studies show that about 40% of the liability toward PD consists of heritable factors. 5-7 Thus far however, the etiology of PD is currently unknown.Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, promotes the survival, differentiation and maintenance of a broad variety of central nervous system neurons. 8,9 BDNF has regulatory effects on multiple neurotransmitter systems, including serotonin 10 and dopamine, 11 and maybe involved in the etiology of stress-related disorders, such as depression and PTSD. Chronic administration of antidepressants, including selective serotonin reuptake inhibitors, increases BDNF expression in the hippocampus. 12 On the other hand, animal studies support the fact that environmental stressors, such as immobilization, decreased central

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BDNF controls dopamine D3 receptor expression and triggers behavioural sensitization

Cited by 521 publications

References 29 publications

BDNF in schizophrenia, depression and corresponding animal models

BDNF in schizophrenia, depression and corresponding animal models

Parental brain‐derived neurotrophic factor genotype, child prosociality, and their interaction as predictors of parents’ warmth

No association between the brain-derived neurotrophic factor gene and panic disorder in Japanese population

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