Brain-derived neurotrophic factor triggers a rapid glutamate release through increase of intracellular Ca2+ and Na+ in cultured cerebellar neurons

2001 ◽  
Vol 66 (1) ◽  
pp. 96-108 ◽  
Author(s):  
T. Numakawa ◽  
T. Matsumoto ◽  
N. Adachi ◽  
D. Yokomaku ◽  
M. Kojima ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Glutamate Release ◽  
Brain Derived Neurotrophic Factor ◽  
Cerebellar Neurons

scholarly journals Chronic Antidepressants Potentiate via Sigma-1 Receptors the Brain-derived Neurotrophic Factor-induced Signaling for Glutamate Release

2006 ◽  
Vol 281 (18) ◽  
pp. 12941-12949 ◽  
Author(s):  
Yuki Yagasaki ◽  
Tadahiro Numakawa ◽  
Emi Kumamaru ◽  
Teruo Hayashi ◽  
Tsung-Ping Su ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Glutamate Release ◽  
Brain Derived Neurotrophic Factor ◽  
Sigma 1 ◽  
The Brain

scholarly journals Presynaptic and Postsynaptic NMDA Receptors Mediate Distinct Effects of Brain-Derived Neurotrophic Factor on Synaptic Transmission

2008 ◽  
Vol 100 (6) ◽  
pp. 3175-3184 ◽  
Author(s):  
Joseph C. Madara ◽  
Eric S. Levine
Keyword(s):  
Synaptic Transmission ◽  
Nmda Receptors ◽  
Neurotrophic Factor ◽  
Developmental Plasticity ◽  
Granule Cells ◽  
Slow Component ◽  
Glutamate Release ◽  
Brain Slices ◽  
Brain Derived Neurotrophic Factor ◽  
Cellular Mechanisms

In addition to its effects on neuronal survival and differentiation, brain-derived neurotrophic factor (BDNF) plays an important role in modulating synaptic transmission and plasticity in many brain areas, most notably the neocortex and hippocampus. These effects may underlie a role for BDNF in learning and memory as well as developmental plasticity. Consistent with localization of the tropomyosin-related kinase B receptor to both sides of the synapse, BDNF appears to have pre- and postsynaptic effects, but the underlying cellular mechanisms are unclear and it is not known whether pre- and postsynaptic modulations by BDNF occur simultaneously. To address these issues, we recorded dual-component (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid [AMPA] and N-methyl-d-aspartate [NMDA]) miniature excitatory postsynaptic currents (mEPSCs) from cortical and hippocampal pyramidal neurons and dentate gyrus granule cells from acute brain slices. BDNF had no effect on the fast component of mEPSC decay or on the peak amplitude, suggesting that BDNF did not modulate postsynaptic AMPA receptors, although BDNF rapidly modulated NMDA receptors, as seen by an enhancement of the slow component of mEPSC decay that was prevented by blocking postsynaptic NMDA receptors. At the same time, BDNF acted presynaptically to enhance mEPSC frequency. Surprisingly, the effect on frequency was also NMDA receptor dependent, but required activation of presynaptic, not postsynaptic, NMDA receptors. BDNF also enhanced action potential–dependent glutamate release via presynaptic NMDA receptors, an effect that was unmasked when voltage-gated calcium channels were partially inhibited. Our results indicate that BDNF acutely modulates presynaptic release and postsynaptic responsiveness through simultaneous effects on pre- and postsynaptic NMDA receptors.

scholarly journals Glucocorticoid Prevents Brain-Derived Neurotrophic Factor-Mediated Maturation of Synaptic Function in Developing Hippocampal Neurons through Reduction in the Activity of Mitogen-Activated Protein Kinase

2008 ◽  
Vol 22 (3) ◽  
pp. 546-558 ◽  
Author(s):  
Emi Kumamaru ◽  
Tadahiro Numakawa ◽  
Naoki Adachi ◽  
Yuki Yagasaki ◽  
Aiko Izumi ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Neurotrophic Factor ◽  
Intracellular Signaling ◽  
Hippocampal Neurons ◽  
Glutamate Release ◽  
Brain Derived Neurotrophic Factor ◽  
Synaptic Function ◽  
Synaptic Proteins ◽  
Mature Stage ◽  
Synaptic Maturation

Abstract An increased level of glucocorticoid may be related to the pathophysiology of depressive disorder. The involvement of brain-derived neurotrophic factor (BDNF) in the antidepressive effect has also been suggested; however, the possible influence of glucocorticoid on the action of BDNF in the developing central nervous system has not been elucidated. In this study, we investigated the effect of glucocorticoid (dexamethasone, DEX) on synaptic maturation and function enhanced by BDNF in early developing hippocampal neurons. In the immature stage, BDNF increased the outgrowth of dendrites and the expression of synaptic proteins including glutamate receptors and presynaptic proteins. Pretreatment with DEX significantly inhibited the BDNF-dependent up-regulation of both dendritic outgrowth and synaptic proteins. In the more mature stage, the BDNF-reinforced postsynaptic Ca2+ influx was decreased by DEX. BDNF-enhanced presynaptic glutamate release was also suppressed. RU486, a glucocorticoid receptor antagonist, canceled the DEX-dependent blocking effect on the action of BDNF. After down-regulation of glucocorticoid receptor by small interfering RNA application, no inhibitory effect of DEX on the BDNF-increased synaptic proteins was observed. Interestingly, the BDNF-activated MAPK/ERK pathway, which is an essential intracellular signaling pathway for the BDNF-increased synaptic proteins, was reduced by DEX. These results suggest that BDNF-mediated synaptic maturation is disturbed after neurons are exposed to high-level glucocorticoid in their development stage.

scholarly journals Brain-derived neurotrophic factor enhances depolarization-evoked glutamate release in cultured cortical neurons

2008 ◽  
Vol 79 (3) ◽  
pp. 522-530 ◽  
Author(s):  
Tomoya Matsumoto ◽  
Tadahiro Numakawa ◽  
Naoki Adachi ◽  
Daisaku Yokomaku ◽  
Satoru Yamagishi ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Cortical Neurons ◽  
Glutamate Release ◽  
Brain Derived Neurotrophic Factor ◽  
Cultured Cortical Neurons

Glutamate release correlates with brain-derived neurotrophic factor and trkB mRNA expression in the CA1 region of rat hippocampus

1996 ◽  
Vol 42 (2) ◽  
pp. 317-327 ◽  
Author(s):  
Torkel Falkenberg ◽  
Nils Lindefors ◽  
Francesca Camilli ◽  
Madis Metsis ◽  
Urban Ungerstedt
Keyword(s):  
Mrna Expression ◽  
Neurotrophic Factor ◽  
Glutamate Release ◽  
Brain Derived Neurotrophic Factor ◽  
Rat Hippocampus ◽  
Ca1 Region

scholarly journals Interactions of Glutamatergic Neurotransmission and Brain-Derived Neurotrophic Factor in the Regulation of Behaviors after Nicotine Administration

2019 ◽  
Vol 20 (12) ◽  
pp. 2943 ◽  
Author(s):  
Jieun Kim ◽  
Ju Hwan Yang ◽  
In Soo Ryu ◽  
Sumin Sohn ◽  
Sunghyun Kim ◽  
...  
Keyword(s):  
Nicotine Dependence ◽  
Nicotinic Acetylcholine Receptors ◽  
Neurotrophic Factor ◽  
Acetylcholine Receptors ◽  
Glutamate Release ◽  
Brain Derived Neurotrophic Factor ◽  
Nicotine Exposure ◽  
Glutamatergic Neurotransmission ◽  
Basal Nuclei ◽  
Nicotine Administration

Nicotine causes tobacco dependence, which may result in fatal respiratory diseases. The striatum is a key structure of forebrain basal nuclei associated with nicotine dependence. In the striatum, glutamate release is increased when α7 nicotinic acetylcholine receptors expressed in the glutamatergic terminals are exposed to nicotine, and over-stimulates glutamate receptors in gamma amino-butyric acid (GABA)ergic neurons. These receptor over-stimulations in turn potentiate GABAergic outputs to forebrain basal nuclei and contribute to the increase in psychomotor behaviors associated with nicotine dependence. In parallel with glutamate increases, nicotine exposure elevates brain-derived neurotrophic factor (BDNF) release through anterograde and retrograde targeting of the synapses of glutamatergic terminals and GABAergic neurons. This article reviews nicotine-exposure induced elevations of glutamatergic neurotransmission, the bidirectional targeting of BDNF in the striatum, and the potential regulatory role played by BDNF in behavioral responses to nicotine exposure.

Acceleration of methylmercury-induced cell death of rat cerebellar neurons by brain-derived neurotrophic factor in vitro

2009 ◽  
Vol 1273 ◽  
pp. 155-162 ◽  
Author(s):  
Motoharu Sakaue ◽  
Naoko Mori ◽  
Misato Makita ◽  
Kana Fujishima ◽  
Shuntaro Hara ◽  
...  
Keyword(s):  
Cell Death ◽  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Cerebellar Neurons
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