BDNF is Upregulated by Postnatal Development and Visual Experience: Quantitative and Immunohistochemical Analyses of BDNF in the Rat Retina

Seki, Masaaki; Nawa, Hiroyuki; Fukuchi, Takeo; Abe, Haruki; Takei, Nobuyuki

doi:10.1167/iovs.02-1089

Cited by 96 publications

(105 citation statements)

References 52 publications

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“…2G). Similar to previous studies in rat (Pollock et al, 2001;Seki et al, 2003;Mandolesi et al, 2005), we also found that the expression level of endogenous retinal BDNF in mice is regulated by visual experience. In DR WT P28 mice, the retinal BDNF mRNA and protein levels were 36.5 Ϯ 6.7% ( p Ͻ 0.001) and 67.5 Ϯ 25.2% ( p ϭ 0.04; Student's t tests) of the levels in age-matched controls raised in 12 h dark/light cycles (NR) (Fig.…”

Section: Bdnf Overexpression Counteracts the Effects Of Visual Deprivsupporting

confidence: 91%

“…In the visual system, maturation controls transcription of BDNF; mRNA levels of BDNF increase in retina and visual cortex after eye opening (Castren et al, 1992;Seki et al, 2003). Dark rearing decreases mRNA levels of BDNF in both of these areas (Castren et al, 1992;Seki et al, 2003;this study).…”

Section: Age-and Experience-dependent Maturation Of Different Subtypementioning

confidence: 89%

“…Retinal proteins were isolated, and Western blots were performed (Johnson et al, 2004). Antibodies against the following proteins were used: BDNF (1:400; Santa Cruz Biotechnology, Santa Cruz, CA) (Seki et al, 2003); protein kinase C (PKC) (1:100; Santa Cruz Biotechnology) (Johnson et al, 2004); Brn-3a (1:100; Chemicon); calretinin (1:1000; Chemicon) (Haverkamp and Wässle, 2000); SMI-32 (1: 1000; Sternberger Monoclonal, Lutherville, MD) (Nixon et al, 1989); glutamic acid decarboxylase (GAD65) (1:100; Hybridoma Bank, Iowa City, IA) (Johnson et al, 2004); calbindin (1:500; Sigma-Aldrich, St. Louis, MO); and glutamate synthetase (1:1000; BD Biosciences, San Jose, CA) (Haverkamp and Wässle, 2000). Calcium-binding protein 5 (CaBP5) (1:500) is a kind gift from Dr. Krzysztof Palczewski at Case Western Reserve University (Cleveland, OH) (Ghosh et al, 2004).…”

Section: Methodsmentioning

confidence: 99%

“…Given that (1) BDNF and TrkB are expressed in the mouse retina (Bennett et al, 1999), (2) visual deprivation reduces levels of retinal BDNF (Seki et al, 2003;Mandolesi et al, 2005;Landi et al, 2007), and (3) BDNF activation of TrkB can regulate neuronal architecture in diverse types of neurons (McAllister et al, 1999;Poo, 2001), we tested the hypothesis that activation of TrkB by BDNF plays a role in maturational and visual experiencedependent refinement of RGC dendrites. This study combined molecular and anatomical analyses of genetically modified mice.…”

Section: Introductionmentioning

confidence: 99%

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Brain-Derived Neurotrophic Factor and TrkB Modulate Visual Experience-Dependent Refinement of Neuronal Pathways in Retina

et al. 2007

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Sensory experience refines neuronal structure and functionality. The visual system has proved to be a productive model system to study this plasticity. In the neonatal retina, the dendritic arbors of a large proportion of ganglion cells are diffuse in the inner plexiform layer. With maturation, many of these arbors become monolaminated. Visual deprivation suppresses this remodeling. Little is known of the molecular mechanisms controlling maturational and experience-dependent refinement. Here, we tested the hypothesis that brainderived neurotrophic factor (BDNF), which is known to regulate dendritic branching and synaptic function in the brain, modulates the developmental and visual experience-dependent refinement of retinal ganglion cells. We used a transgenic mouse line, in which a small number of ganglion cells were labeled with yellow fluorescence protein, to delineate their dendritic structure in vivo. We found that transgenic overexpression of BDNF accelerated the laminar refinement of ganglion cell dendrites, whereas decreased TrkB expression or retina-specific deletion of TrkB, the cognate receptor for BDNF, retarded it. BDNF-TrkB signaling regulated the maturational formation of new branches in ON but not the bilaminated ON-OFF ganglion cells. Furthermore, BDNF overexpression overrides the requirement for visual inputs to stimulate laminar refinement and dendritic branching of ganglion cells. These experiments reveal a previously unrecognized action of BDNF and TrkB in controlling cell-specific, experience-dependent remodeling of neuronal structures in the visual system.

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Section: Bdnf Overexpression Counteracts the Effects Of Visual Deprivsupporting

confidence: 91%

Section: Age-and Experience-dependent Maturation Of Different Subtypementioning

confidence: 89%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Brain-Derived Neurotrophic Factor and TrkB Modulate Visual Experience-Dependent Refinement of Neuronal Pathways in Retina

et al. 2007

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“…RT-PCR-RNA extraction and RT-PCR were performed as previously described (26). Total RNA (100 ng) was amplified using the RT-PCR High Plus Kit (TOYOBO, Japan) with specific primers for rat eEF2 (forward, 5Ј-cgcttctatgccttcggtag-3Ј, reverse, 5Ј-gcagcatcaccagacttcaa-3Ј).…”

Section: Methodsmentioning

confidence: 99%

Brain-derived Neurotrophic Factor Enhances the Basal Rate of Protein Synthesis by Increasing Active Eukaryotic Elongation Factor 2 Levels and Promoting Translation Elongation in Cortical Neurons

Takei

Kawamura

Ishizuka

et al. 2009

Journal of Biological Chemistry

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The constitutive and activity-dependent components of protein synthesis are both critical for neural function. Although the mechanisms controlling extracellularly induced protein synthesis are becoming clear, less is understood about the molecular networks that regulate the basal translation rate. Here we describe the effects of chronic treatment with various neurotrophic factors and cytokines on the basal rate of protein synthesis in primary cortical neurons. Among the examined factors, brain-derived neurotrophic factor (BDNF) showed the strongest effect. The rate of protein synthesis increased in the cortical tissues of BDNF transgenic mice, whereas it decreased in BDNF knock-out mice. BDNF specifically increased the level of the active, unphosphorylated form of eukaryotic elongation factor 2 (eEF2). The levels of active eEF2 increased and decreased in BDNF transgenic and BDNF knock-out mice, respectively. BDNF decreased kinase activity and increased phosphatase activity against eEF2 in vitro. Additionally, BDNF shortened the ribosomal transit time, an index of translation elongation. In agreement with these results, overexpression of eEF2 enhanced protein synthesis. Taken together, our results demonstrate that the increased level of active eEF2 induced by chronic BDNF stimulation enhances translational elongation processes and increases the total rate of protein synthesis in neurons.The synthesis and post-translational modification of proteins play key roles in neural development, synaptic plasticity, and cognitive brain functions such as learning and memory (1, 2). Recent studies have revealed that activity-dependent regulation of translation affects neural plasticity (3, 4). Previously, we reported that BDNF, 2 a critical molecule for neural plasticity (5-7), enhances protein synthesis and activates the translational machinery in central nervous system neurons (8). In addition, neurotransmitters such as glutamate (9, 10), dopamine (11), and serotonin (12) are also reported to facilitate translation in neurons. These observations indicate that endogenous molecules can acutely modulate neuronal translation in response to neural activity. Translation of an mRNA molecule comprises three steps: initiation, elongation, and release (or termination) (13). In the first step, mRNA and methionyltRNA i Met are recruited to a ribosome. During elongation, aminoacyl-tRNAs are sequentially recruited and the nascent peptide chain lengthens incrementally as amino acids are covalently attached via peptide bonds. Finally, the polypeptide chain is released from the ribosome. Each step is regulated by a variety of factors. The activities of these regulatory proteins are predominantly controlled by phosphorylation and GTP binding. BDNF activates both initiation and elongation by modulating these processes (8,14,15).In addition to these acute, stimulation-induced changes in the translation rate, the long term regulation of translation plays important roles in developing and mature brains. In fact, recent studies have shown that ge...

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Percutaneous treatment of a popliteal bifurcation—The value of coronary devices and strategies

Colantonio¹,

Latib²,

Sangiorgi³

2008

Cathet Cardio Intervent

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BDNF is Upregulated by Postnatal Development and Visual Experience: Quantitative and Immunohistochemical Analyses of BDNF in the Rat Retina

Abstract: These observations indicate that BDNF expression in RGCs is upregulated in an activity-dependent manner, whereas that in Müller cells is regulated only by development.

Cited by 96 publications

References 52 publications

Brain-Derived Neurotrophic Factor and TrkB Modulate Visual Experience-Dependent Refinement of Neuronal Pathways in Retina

Brain-Derived Neurotrophic Factor and TrkB Modulate Visual Experience-Dependent Refinement of Neuronal Pathways in Retina

Brain-derived Neurotrophic Factor Enhances the Basal Rate of Protein Synthesis by Increasing Active Eukaryotic Elongation Factor 2 Levels and Promoting Translation Elongation in Cortical Neurons

Percutaneous treatment of a popliteal bifurcation—The value of coronary devices and strategies

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