Temporal and spatial differences in expression of TrkB isoforms in rat retina during constant light exposure

Asai, Nobuharu; Abe, Toshiaki; Saito, Takato; Sato, Hajime; Ishiguro, Sei-ichi; Nishida, Kohji

doi:10.1016/j.exer.2007.05.010

Cited by 17 publications

(13 citation statements)

References 26 publications

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“…8D). Data are in agreement with previous studies that showed that Mu¨ller cells express predominantly truncated TrkB (Asai et al, 2007). Data are also in agreement with studies that showed that, in the brain, truncated TrkB is expressed in neurons and macroglial cells, and that full-length TrkB is expressed almost exclusively in neurons (Klein et al, 1991;Frisen et al, 1993;Ohira et al, 2005).…”

Section: Discussionsupporting

confidence: 93%

“…In the retina, the neurotrophic effect of BDNF is in part mediated by a direct action on retinal neurons, e.g., TrkB-expressing retinal ganglion cells and dopaminergic amacrines (Cellerino and Kohler, 1997;Suzuki et al, 1998;Hirsch et al, 2000;Asai et al, 2007), and by an indirect mechanism involving Mu¨ller cells (Wexler et al, 1998;Wahlin et al, 2000Wahlin et al, , 2001Harada et al, 2002;Saito et al, 2009). However, it was shown that TrkB signaling in Mu¨ller cells, but not in retinal ganglion and amacrine cells, is critically involved in neural protection and regeneration during retinal degeneration (Harada et al, 2011) and that the BDNF-induced protection of photoreceptors from light damage is mediated by activation of truncated TrkB expressed by Mu¨ller cells (Saito et al, 2009).…”

Section: Discussionmentioning

confidence: 95%

“…Likewise, BDNF cannot exert its effects directly on most photoreceptors of the rat retina because they do not express BDNF receptors (Suzuki et al, 1998;Wahlin et al, 2001;Asai et al, 2007). TrkB is expressed by green-red cones (Di Polo et al, 2000;Grishanin et al, 2008) which represent less than 1% of all photoreceptors of the rat retina (Sze´l and Ro¨hlich, 1992).…”

Section: Introductionmentioning

confidence: 97%

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Brain-derived neurotrophic factor inhibits osmotic swelling of rat retinal glial (Müller) and bipolar cells by activation of basic fibroblast growth factor signaling

et al. 2015

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 97%

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Brain-derived neurotrophic factor inhibits osmotic swelling of rat retinal glial (Müller) and bipolar cells by activation of basic fibroblast growth factor signaling

et al. 2015

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“…Amplifications were performed in a total volume of 20 μl with 40 nMol primers for each reaction on an Opticon MJ Thermocycler; MJ Research (Watertown, MA). The following published primer sequences were used: Bdnf exons I, II, II, and (Tsankova et al, 2006) Bdnf total (Asai et al, 2007), and Drd3 and Gapdh (Andersen et al, 2008). …”

Section: Methodsmentioning

confidence: 99%

Juvenile methylphenidate reduces prefrontal cortex plasticity via D3 receptor and BDNF in adulthood

Andersen

Sonntag

2014

Front. Synaptic Neurosci.

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Background: Early drug intervention in childhood disorders aims to maximize individual potential in the short- and long-term. Consistently, juvenile exposure to psychostimulants, such as methylphenidate (MPH), reduces risk for substance use in animals and sub-populations of individuals with attention deficit hyperactivity disorder (ADHD). We investigated the effects of MPH on brain plasticity via dopamine receptor D3 (D3R) and brain-derived neurotrophic factor (BDNF) expression in developing rats.Methods: Between postnatal days 20–35, rat pups were administered saline vehicle (Veh) or MPH (2 mg/kg), the D3R-preferring agonist ±7-OHDPAT, or the antagonist nafadotride (0.05 mg/kg) alone, or in combination with MPH twice a day. In adulthood, subjects were challenged to Veh or cocaine (10 mg/kg for two days). The prefrontal cortex was analyzed for protein and mRNA levels of total BDNF, its splice variants I, IIc, III/IV, and IV/VI, and D3 receptors. A separate group of subjects was assessed for splice variants at 20, 35, 40, and 60 days of age.Results: Across age strong correlations were evident between Drd3 and Bdnf mRNA levels (r = 0.65) and a negative relationship between Drd3 and exon IIc after MPH treatment (r = −0.73). BDNF protein levels did not differ between Veh- and MPH subjects at baseline, but were significantly lower in MPH-treated and cocaine challenged subjects (30.3 ± 9.7%). Bdnf mRNA was significantly higher in MPH-treated subjects, and reversed upon exposure to cocaine. This effect was blocked by nafadotride. Furthermore, Bdnftotal and Bdnf splice variants I, IIc, III/IV, and IV/VI changed across the transitions between juvenility and late adolescence.Conclusions: These data suggest a sensitive window of vulnerability to modulation of BDNF expression around adolescence, and that compared to normal animals, juvenile exposure to MPH permanently reduces prefrontal BDNF transcription and translation upon cocaine exposure in adulthood by a D3R-mediated mechanism.

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“…RNA was extracted from brain tissue (sham (n03); sham+hucb (n03); lesion (n03); lesion+hucb (n0 3)), and reversed transcribed three times independently. Primers for real time PCR were as follows: BDNFupstream primer (USP): 5'-actctggagagcgtgaatgg-3' (Asai et al 2007), BDNF-downstream primer (DSP): 5'-tccaaagg cacttgactgct-3', VEGF-USP: 5'-acgaaagcgcaagaaatccc-3', VEGF-DSP: 5'-tgcaacgcgagtctgtgttt-3', 18S-USP: 5'-agaacgaaagtcggaggttcg-3', 18S-DSP: 5'-tgagtcaaattaagccg cagg-3'. The rat specific VEGF primer sequences were according to Wakabayashi et al (2010).…”

Section: Quantitative Real Time Polymerase Chain Reactionmentioning

confidence: 99%

Transplantation of human umbilical cord blood cells mediated beneficial effects on apoptosis, angiogenesis and neuronal survival after hypoxic-ischemic brain injury in rats

et al. 2012

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Transplantation of human umbilical cord blood (hucb) cells in a model of hypoxic-ischemic brain injury led to the amelioration of lesion-impaired neurological and motor functions. However, the mechanisms by which transplanted cells mediate functional recovery after brain injury are largely unknown. In this study, the effects of hucb cell transplantation were investigated in this experimental paradigm at the cellular and molecular level. As the pathological cascade in hypoxic-ischemic brain injury includes inflammation, reduced blood flow, and neuronal cell death, we analyzed the effects of peripherally administered hucb cells on these detrimental processes, investigating the expression of characteristic marker proteins. Application of hucb cells after perinatal hypoxic-ischemic brain injury correlated with an increased expression of the proteins Tie-2 and occludin, which are associated with angiogenesis. Lesion-induced apoptosis, determined by expression of cleaved caspase-3, decreased, whereas the number of vital neurons, identified by counting of NeuN-positive cells, increased. In addition, we observed an increase in the expression of neurotrophic and pro-angiogenic growth factors, namely BDNF and VEGF, in the lesioned brain upon hucb cell transplantation. The release of neurotrophic factors mediated by transplanted hucb cells might cause a lower number of neurons to undergo apoptosis and result in a higher number of living neurons. In parallel, the increase of VEGF might cause growth of blood vessels. Thus, hucb transplantation might contribute to functional recovery after brain injury mediated by systemic or local effects.

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Temporal and spatial differences in expression of TrkB isoforms in rat retina during constant light exposure

Cited by 17 publications

References 26 publications

Brain-derived neurotrophic factor inhibits osmotic swelling of rat retinal glial (Müller) and bipolar cells by activation of basic fibroblast growth factor signaling

Brain-derived neurotrophic factor inhibits osmotic swelling of rat retinal glial (Müller) and bipolar cells by activation of basic fibroblast growth factor signaling

Juvenile methylphenidate reduces prefrontal cortex plasticity via D3 receptor and BDNF in adulthood

Transplantation of human umbilical cord blood cells mediated beneficial effects on apoptosis, angiogenesis and neuronal survival after hypoxic-ischemic brain injury in rats

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