Examination of behavioral deficits triggered by targeting BDNF in fetal or postnatal brains of mice

Chan, Jason P.; Unger, Thaddeus J.; Byrnes, John; Rios, Maribel

doi:10.1016/j.neuroscience.2006.06.002

Cited by 121 publications

(85 citation statements)

References 52 publications

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“…The lack of better behavioral assays could also be contributing to confounding the ability to determine whether and to what extent BDNF is involved in depression, the antidepressant response and/or in anxiety. It should be noted, however, that two recent studies have shown 'depressive like' behaviors in two separate sets of BDNF conditional mouse lines, using the FTS and the TST (Chan et al, 2006;Monteggia et al, 2007). Thus, further studies are necessary to sort out the conflicting results, and establish that BDNF signaling (or lack of) does not contribute directly 'depressive-like' behaviors per se.…”

Section: Bdnf Mutant Micementioning

confidence: 99%

Interaction between BDNF and Serotonin: Role in Mood Disorders

Martinowich

2007

Neuropsychopharmacol

675

458

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Brain-derived neurotrophic factor (BDNF) and serotonin (5-hydroxytryptamine, 5-HT) are two seemingly distinct signaling systems that play regulatory roles in many neuronal functions including survival, neurogenesis, and synaptic plasticity. A common feature of the two systems is their ability to regulate the development and plasticity of neural circuits involved in mood disorders such as depression and anxiety. BDNF promotes the survival and differentiation of 5-HT neurons. Conversely, administration of antidepressant selective serotonin reuptake inhibitors (SSRIs) enhances BDNF gene expression. There is also evidence for synergism between the two systems in affective behaviors and genetic epitasis between BDNF and the serotonin transporter genes.

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Section: Bdnf Mutant Micementioning

confidence: 99%

Interaction between BDNF and Serotonin: Role in Mood Disorders

Martinowich

2007

Neuropsychopharmacol

675

458

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“…[192][193][194] Work with mouse lines characterized by deficient Bdnf has shown that these trophic effects are important for normal serotonergic neurotransmission. [195][196][197][198][199][200] In addition, several lines of evidence have provided support for a role of Mecp2 in the regulation of activity-dependent transcription of Bdnf, 134,201,202 suggesting that alterations in 5-HT signaling could arise from deficient Mecp2 function, through dysregulation of Bdnf. Bdnf-null mice die soon after birth, but mutants have been developed with conditional disruption of Bdnf, limited to either the prenatal or postnatal period.…”

Section: Autism Candidate Genes and Synaptic Functionmentioning

confidence: 99%

“…Bdnf-null mice die soon after birth, but mutants have been developed with conditional disruption of Bdnf, limited to either the prenatal or postnatal period. 196 The conditional null mice demonstrate significant behavioral changes, including marked hyperactivity and enhanced aggression, as well as selective deficits in serotonergic neurotransmission. 196,203 One study has reported that the behavioral effects of Bdnf disruption in forebrain, whether in late embryogenesis or during the postnatal period, are dependent on gender, with only male conditional null mice showing increases in activity, and only female mutants exhibiting depression-like responses, measured as greater immobility in a forced swim test.…”

Section: Autism Candidate Genes and Synaptic Functionmentioning

confidence: 99%

“…196 The conditional null mice demonstrate significant behavioral changes, including marked hyperactivity and enhanced aggression, as well as selective deficits in serotonergic neurotransmission. 196,203 One study has reported that the behavioral effects of Bdnf disruption in forebrain, whether in late embryogenesis or during the postnatal period, are dependent on gender, with only male conditional null mice showing increases in activity, and only female mutants exhibiting depression-like responses, measured as greater immobility in a forced swim test. 204 Monteggia et al 205 used an inducible Bdnf-null mutation to compare forebrain-specific neurotrophin loss during development and in adulthood.…”

Section: Autism Candidate Genes and Synaptic Functionmentioning

confidence: 99%

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Advances in behavioral genetics: mouse models of autism

2007

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Autism is a neurodevelopmental syndrome with markedly high heritability. The diagnostic indicators of autism are core behavioral symptoms, rather than definitive neuropathological markers. Etiology is thought to involve complex, multigenic interactions and possible environmental contributions. In this review, we focus on genetic pathways with multiple members represented in autism candidate gene lists. Many of these pathways can also be impinged upon by environmental risk factors associated with the disorder. The mouse model system provides a method to experimentally manipulate candidate genes for autism susceptibility, and to use environmental challenges to drive aberrant gene expression and cell pathology early in development. Mouse models for fragile X syndrome, Rett syndrome and other disorders associated with autistic-like behavior have elucidated neuropathology that might underlie the autism phenotype, including abnormalities in synaptic plasticity. Mouse models have also been used to investigate the effects of alterations in signaling pathways on neuronal migration, neurotransmission and brain anatomy, relevant to findings in autistic populations. Advances have included the evaluation of mouse models with behavioral assays designed to reflect disease symptoms, including impaired social interaction, communication deficits and repetitive behaviors, and the symptom onset during the neonatal period. Research focusing on the effect of gene-by-gene interactions or genetic susceptibility to detrimental environmental challenges may further understanding of the complex etiology for autism.

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“…We investigated the role of BDNF because it has been implicated in the development of synaptic architecture throughout development (i.e., Chan et al, 2006;Bao et al, 1999;Liou et al;1997;Martinez et al, 1998;Wang et al, 1995) and thus has the potential to be affected by drug insults. In addition, in the adult animal, BDNF has been implicated in changes in plasticity associated with drug exposure, escalation, and abuse (reviewed by Bolanos and Nestler, 2005; see also Berglind et al, 2007;Cheng et al, 2005;Tsai et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Prenatal opiate exposure impairs radial arm maze performance and reduces levels of BDNF precursor following training

2008

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Prenatal exposure to opiates, which is invariably followed by postnatal withdrawal, can affect cognitive performance. To further characterize these effects, we examined radial 8-arm maze performance and expression of brain derived neurotrophic factor (BDNF) in male rats prenatally exposed to the opiate l-α-acetylmethadol (LAAM). Female rats received 1.0 mg/kg/day LAAM or water via daily oral gavage for 28 days prior to breeding, during breeding, and throughout pregnancy. Pups were fostered to non-treated lactating dams at birth and underwent neonatal opiate withdrawal. At 5-6 months, prenatal water-and LAAM-exposed males (n=6 each; non-littermates) received radial arm maze training consisting of ten trials a day for five days and three retention trials on day six. Rats prenatally exposed to LAAM had poorer maze performance, decreased percent correct responding and more reference and working memory errors than prenatal water-treated controls. However, they were able to acquire the task by the end of training. There were no differences between the groups on retention 24 hr after testing. Following retention testing, hippocampi were removed and protein extracted from cytosol and synaptic fractions. Western blots were used to measure levels of mature and precursor BDNF protein, as well as the BDNF receptor TrkB. BDNF precursor protein was significantly decreased in the synaptic fraction of trained prenatal LAAM-treated rats compared to prenatal water-treated trained controls. No effects were found for the full-length or truncated TrkB receptor. In untrained rats, prenatal treatment did not affect any of the measures. These data suggest that prenatal opiate exposure and/or postnatal withdrawal compromise expression of proteins involved in the neural plasticity underlying learning.

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Examination of behavioral deficits triggered by targeting BDNF in fetal or postnatal brains of mice

Cited by 121 publications

References 52 publications

Interaction between BDNF and Serotonin: Role in Mood Disorders

Interaction between BDNF and Serotonin: Role in Mood Disorders

Advances in behavioral genetics: mouse models of autism

Prenatal opiate exposure impairs radial arm maze performance and reduces levels of BDNF precursor following training

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