Differential Activation of Brain-derived Neurotrophic Factor Gene Promoters I and III by Ca2+ Signals Evoked vial-type Voltage-dependent andN-Methyl-d-aspartate Receptor Ca2+Channels

Tabuchi, Akiko; Nakaoka, Ryuki; Amano, Kenji; Yukimine, Masaru; Andoh, Tsugunobu; Kuraishi, Yasushi; Tsuda, Masashi

doi:10.1074/jbc.m909538199

Cited by 128 publications

(119 citation statements)

References 25 publications

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“…This effect is in agreement with changes reported following immobilization stress at a similar time point (Marmigere et al, 2003), although longer stressors appear to be ineffective or even inhibitory on its transcription (Marmigere et al, 2003;Nair et al, 2007). BDNF exon IV is highly responsive to neuronal activation and its expression is upregulated under different experimental conditions, through the activation of calcium and cAMP responsive element (Tabuchi et al, 2000). CREB does not appear to contribute to this effect although, as our analysis was limited to a single time point, the possibility exits that changes in CREB activation may occur earlier Figure 5 Effect of acute swim stress on glucocorticoid receptor protein levels in the cytosolic (a) and nuclear (b) compartments obtained from the hippocampus of rats chronically treated with duloxetine (DLX; 10 mg/kg) or vehicle (VEH) and killed 15 min after the end of the stress session.…”

Section: Stress-dependent Bdnf Modulation After Duloxetine R Molteni supporting

confidence: 79%

“…It has been reported that the regulation of BDNF exon IV depends primarily on the activity of Ca 2 + and CREB (Tabuchi et al, 2000(Tabuchi et al, , 2002Tao et al, 2002), which stimulate exon IV transcription, as well as on MeCP2 that represses it (Chen et al, 2003;Zhou et al, 2006). Hence, we investigated their expression (total levels) and activation (phosphorylated levels) in response to DLX treatment as well as to acute stress.…”

Section: Analysis Of Proteins Involved In Bdnf Transcriptionmentioning

confidence: 99%

“…To address the potential mechanisms underling transcriptional changes of BDNF, we investigated the expression of specific proteins that are involved in the regulation of BDNF exons IV and VI promoters, which have been studied in detail (Tabuchi et al, 2000(Tabuchi et al, , 2002Takeuchi et al, 2000Takeuchi et al, , 2002. It has been reported that the regulation of BDNF exon IV depends primarily on the activity of Ca 2 + and CREB (Tabuchi et al, 2000(Tabuchi et al, , 2002Tao et al, 2002), which stimulate exon IV transcription, as well as on MeCP2 that represses it (Chen et al, 2003;Zhou et al, 2006).…”

Section: Analysis Of Proteins Involved In Bdnf Transcriptionmentioning

confidence: 99%

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Acute Stress Responsiveness of the Neurotrophin BDNF in the Rat Hippocampus is Modulated by Chronic Treatment with the Antidepressant Duloxetine

Molteni

Calabrese

Cattaneo

et al. 2008

Neuropsychopharmacol

115

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Compelling evidence suggests that mood disorders are characterized by reduced neuronal plasticity that might be normalized by pharmacological intervention. Our study aimed to establish whether chronic antidepressant treatment could alter the modulation of the neurotrophin brain-derived neurotrophic factor (BDNF) under a stressful condition. Therefore, adult male Sprague-Dawley rats were treated for 21 days with vehicle or with the SNRI duloxetine and, 24 h after the last injection, exposed to an acute swim stress (5 min) before being killed 15 min later. We found that chronic duloxetine treatment was able to modulate the rapid transcriptional changes of BDNF isoforms produced by an acute swim stress. Indeed whereas the mRNA levels of BDNF exon IV were upregulated by stress in vehicle as well as in duloxetine-treated rats, a significant increase of exon VI and exon IX was only found in rats that were pretreated with the antidepressant. These differential effects are in part because of selective changes in signaling pathways involved in the control of BDNF transcription. Moreover, the acute stressful episode significantly increased the levels of mature BDNF protein in the synaptosomal compartment in rats that were pretreated with the antidepressant, but not in control animals. Our results suggest that chronic antidepressant treatment might affect the responsiveness of BDNF under stressful conditions, suggesting that pharmacological intervention could 'prime' neuroprotective pathways and render them more responsive to preserve cell function and viability.

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Section: Stress-dependent Bdnf Modulation After Duloxetine R Molteni supporting

confidence: 79%

Section: Analysis Of Proteins Involved In Bdnf Transcriptionmentioning

confidence: 99%

Section: Analysis Of Proteins Involved In Bdnf Transcriptionmentioning

confidence: 99%

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Acute Stress Responsiveness of the Neurotrophin BDNF in the Rat Hippocampus is Modulated by Chronic Treatment with the Antidepressant Duloxetine

Molteni

Calabrese

Cattaneo

et al. 2008

Neuropsychopharmacol

115

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“…Calcium entry through L-type channels has been shown to play an important role in activity-dependent BDNF expression in hippocampal neurons (Zafra et al, 1990(Zafra et al, , 1991Ghosh et al, 1994;Tabuchi et al, 2000). Therefore, to determine whether calcium entry through L-type channels is capable of regulating release of native BDNF from hippocampal neurons, we exposed hippocampal cultures to 5 M Bay K-8644, a selective agonist of L-type channels (Nowycky et al, 1985;Brosenitsch et al, 1998), in the presence of 15 mM KCl, a protocol that optimizes the efficacy of Bay K-8644 by slightly depolarizing the cells (Brosenitsch et al, 1998).…”

Section: Release Of Native Bdnf Evoked By Patterned Electrical Stimulmentioning

confidence: 99%

Cellular Mechanisms Regulating Activity-Dependent Release of Native Brain-Derived Neurotrophic Factor from Hippocampal Neurons

2002

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Brain-derived neurotrophic factor (BDNF) plays a critical role in activity-dependent modifications of neuronal connectivity and synaptic strength, including establishment of hippocampal long-term potentiation (LTP). To shed light on mechanisms underlying BDNF-dependent synaptic plasticity, the present study was undertaken to characterize release of native BDNF from newborn rat hippocampal neurons in response to physiologically relevant patterns of electrical field stimulation in culture, including tonic stimulation at 5 Hz, bursting stimulation at 25 and 100 Hz, and theta-burst stimulation (TBS). Release was measured using the ELISA in situ technique, developed in our laboratory to quantify secretion of native BDNF without the need to first overexpress the protein to nonphysiological levels. Each stimulation protocol resulted in a significant increase in BDNF release that was tetrodotoxin sensitive and occurred in the absence of glutamate receptor activation. However, 100 Hz tetanus and TBS, stimulus patterns that are most effective in inducing hippocampal LTP, were significantly more effective in releasing native BDNF than lower-frequency stimulation. For all stimulation protocols tested, removal of extracellular calcium, or blockade of N-type calcium channels, prevented BDNF release. Similarly, depletion of intracellular calcium stores with thapsigargin and treatment with dantrolene, an inhibitor of calcium release from caffeine-ryanodine-sensitive stores, markedly inhibited activity-dependent BDNF release. Our results indicate that BDNF release can encode temporal features of hippocampal neuronal activity. The dual requirement for calcium influx through N-type calcium channels and calcium mobilization from intracellular stores strongly implicates a role for calcium-induced calcium release in activity-dependent BDNF secretion.

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“…Because the survival component of postnatal hippocampal neurogenesis is regulated in part by the neurotrophic agent brain-derived neurotrophic factor (BDNF), 19 and LTCC-signaling controls BDNF expression in in vitro systems, 20,21 we measured BDNF protein levels in forebrain Ca v 1.2 cKO mice. Here, we observed a 50% reduction relative to age / sex-matched WT littermates ( Fig.…”

mentioning

confidence: 99%

Cacna1c: Protecting young hippocampal neurons in the adult brain

2016

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Differential Activation of Brain-derived Neurotrophic Factor Gene Promoters I and III by Ca2+ Signals Evoked vial-type Voltage-dependent andN-Methyl-d-aspartate Receptor Ca2+Channels

Cited by 128 publications

References 25 publications

Acute Stress Responsiveness of the Neurotrophin BDNF in the Rat Hippocampus is Modulated by Chronic Treatment with the Antidepressant Duloxetine

Acute Stress Responsiveness of the Neurotrophin BDNF in the Rat Hippocampus is Modulated by Chronic Treatment with the Antidepressant Duloxetine

Cellular Mechanisms Regulating Activity-Dependent Release of Native Brain-Derived Neurotrophic Factor from Hippocampal Neurons

Cacna1c: Protecting young hippocampal neurons in the adult brain

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