Brain-derived neurotrophic factor regulates early postnatal developmental cell death of dopamine neurons of the substantia nigra in vivo

Oo, Tinmarla F.; Marchionini, Deanna; Yarygina, Olga; O’Leary, Paul D.; Hughes, Richard A.; Kholodilov, Nikolai; Burke, Robert E.

doi:10.1016/j.mcn.2009.04.009

Cited by 25 publications

(13 citation statements)

References 50 publications

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“…The secreted factors GDNF and BDNF and the transcription factor Pitx3 are individually required for the proper development of mdDA neurons or for their survival during postnatal and adult stages (Baquet et al, 2005;Smidt and Burbach, 2007;Pascual et al, 2008;Oo et al, 2009), but it remained unclear whether a regulatory interaction exists between these three factors during embryonic development or in the adult brain. Here we show that NF-B-mediated GDNF/Ret signaling is, at least in part, sufficient for the activation of Pitx3 expression, which is in turn required for the transcription of BDNF in a rostrolateral and medial mdDA neuronal subpopulation, thereby promoting the survival of these neurons during mouse embryonic development (Fig.…”

Section: Discussionmentioning

confidence: 99%

Pitx3 Is a Critical Mediator of GDNF-Induced BDNF Expression in Nigrostriatal Dopaminergic Neurons

Peng¹,

Aron²,

Klein³

et al. 2011

J. Neurosci.

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Ϫ/Ϫ mdDA neurons. Most importantly, only BDNF but not GDNF protects mdDA neurons against 6-hydroxydopamine-induced cell death in the absence of Pitx3. As the feedforward regulation of GDNF, Pitx3, and BDNF expression also persists in the adult rodent brain, our data suggest that the disruption of the regulatory interaction between these three factors contributes to the loss of mdDA neurons in Pitx3 Ϫ/Ϫ mutant mice and perhaps also in human PD.

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Section: Discussionmentioning

confidence: 99%

Pitx3 Is a Critical Mediator of GDNF-Induced BDNF Expression in Nigrostriatal Dopaminergic Neurons

Peng¹,

Aron²,

Klein³

et al. 2011

J. Neurosci.

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“…With respect to the role of BDNF in dopaminergic systems, recent studies show that BDNF facilitates maturation of mesenchymal stem cell-derived dopamine progenitors to functional neurons (Trzaska et al 2009) and modulates cell death in the substantia nigra (Oo et al 2009). BDNF therefore seems to play a key role in the development of dopamine system in the brain.…”

Section: Discussionmentioning

confidence: 99%

Val/Val genotype of brain-derived neurotrophic factor (BDNF) Val66Met polymorphism is associated with a better response to OROS-MPH in Korean ADHD children

Kim

Cummins

Kim

et al. 2011

Int. J. Neuropsychopharm.

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Research on psychostimulants, analysis of animal models and genetic association studies all suggest that the brain-derived neurotrophic factor gene (BDNF) may be a good candidate for pharmacogenetic studies of attention deficit hyperactivity disorder (ADHD). Yet to date there have been no pharmacogenetic studies of BDNF in ADHD. A total of 102 drug-naive ADHD children (8.7±2.1 yr) were treated with osmotic release oral system-methylphenidate (OROS-MPH) for 12 wk, and four kinds of response criteria were applied, based first, on a combined threshold of the ADHD Rating Scale - IV (ARS) and the Clinical Global Impression - Improvement scale (CGI-I); second, on scores of 1 or 2 vs. 3-7 on the CGI - Severity scale; third, on a >50% reduction in ARS scores; and fourth, on satisfaction of all of the aforementioned criteria. The Val⁶⁶Met polymorphism of BDNF and six single nucleotide polymorphisms from the SLC6A2, ADRA2A and NTF-3 genes were tested for association with each criterion. Relative to other genotypes, homozygosity for the Val allele of the BDNF Val⁶⁶Met polymorphism was associated with a greater relative frequency of good response under all four response criteria (after controlling for baseline ARS score, age, gender, final dose (mg/kg) of OROS-MPH at 12 wk, and level of academic functioning). This association was significant at the uncorrected level for the first and third response criteria (p=0.013 and p=0.018, respectively) and significant at a Bonferroni-corrected level for the second and fourth response criteria (p=0.0002, p=0.0003, respectively). Our findings support an association between homozygosity for the Val allele of BDNF and better response to OROS-MPH in Korean ADHD children as assessed by four different response criteria.

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“…[27][28][29] Further, regulation of the DAergic development is mediated by other neurotrophic factors, including BDNF, 11 which promotes sprouting of DAergic axons and regulates plasticity of the DAergic neurons. 84 Studies also showed that psychostimulant-induced enhancement of DA transmission 35 and TH at the DAergic terminals mediated through NOS gene. 85 Moreover, NT-induced cell degeneration is thought to be involved in NT autoxidation and disruption of the cellular redox system.…”

Section: -64mentioning

confidence: 99%

Involvement of Neurotransmitter and Nrf2 in Nicotine- and Cigarette Smoke-Induced Testicular Toxicity in Adult Rats

2016

Reproductive Biology Insights

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Several organ systems can be affected by nicotine/cigarette smoking (CS); however, there is a gap of knowledge about the role of local neurotransmitter system, brain-derived neurotrophic factor (BDNF), and dopamine (DA) in testicular toxicity. Therefore, the aim of the present study is to explore the toxic impact of short-and long-term exposure to oral nicotine and passive CS on adult albino Wistar rats, using doses that closely mimic the human smoking scenario. Our results showed dose-and time-dependent loss of developing spermatogonia and spermatocyte of the seminiferous tubules, disruption of basement membrane, DNA damage, and high serum cotinine upon exposure to nicotine and CS, resulting in low sperm count as compared to control. Further, the results showed the upregulation of BDNF, DA, tyrosine hydroxylase (TH), and pro-oxidants, ie, reactive oxygen species (ROS) and inducible nitric oxide synthetase (iNOS), in the exposed testis and downregulation of the antioxidants such as, ascorbate and Nrf2 when compared with the control. Thus, our results for the first time highlight a potential role of the local neurotransmitter system and antioxidant depletion (Nrf2) in nicotine/ CS-induced testicular pathogenesis, which could underpin the development of therapeutic interventions targeted at oxidative stress-associated disorders, and probably establish a link with the brain system contributing to addiction.KEY WORDS: nicotine, cigarette smoking, dopamine, BDNF, testis, Nrf2, oxidative stress, molecular mechanism CITATION: naha et al. involvement of neurotransmitter and nrf2 in nicotine-and cigarette smoke-induced testicular toxicity in Adult Rats.

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Brain-derived neurotrophic factor regulates early postnatal developmental cell death of dopamine neurons of the substantia nigra in vivo

Cited by 25 publications

References 50 publications

Pitx3 Is a Critical Mediator of GDNF-Induced BDNF Expression in Nigrostriatal Dopaminergic Neurons

Pitx3 Is a Critical Mediator of GDNF-Induced BDNF Expression in Nigrostriatal Dopaminergic Neurons

Val/Val genotype of brain-derived neurotrophic factor (BDNF) Val66Met polymorphism is associated with a better response to OROS-MPH in Korean ADHD children

Involvement of Neurotransmitter and Nrf2 in Nicotine- and Cigarette Smoke-Induced Testicular Toxicity in Adult Rats

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