Brain-derived Neurotrophic Factor Regulates Surface Expression of α-Amino-3-hydroxy-5-methyl-4-isoxazoleproprionic Acid Receptors by Enhancing the N-Ethylmaleimide-sensitive Factor/GluR2 Interaction in Developing Neocortical Neurons

Narisawa‐Saito, Mako; Iwakura, Yuriko; Kawamura, Minoru; Araki, Kazuo; Kozaki, Shunji; Takei, Nobuyuki; Nawa, Hiroyuki

doi:10.1074/jbc.m202158200

Cited by 94 publications

(82 citation statements)

References 57 publications

(74 reference statements)

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“…Subchronic treatment with BDNF up-regulates the expression and activity of AMPA receptor channels in GABAergic neocortical neurons in culture (Narisawa-Saito et al, 2002;Nagano et al, 2003). The present results revealed an opposing activity of TGFα, reducing the expression and activity of AMPA receptor channels.…”

Section: Antagonistic Effects Of Tgfα Against Bdnfsupporting

confidence: 54%

“…In addition, BDNF effects on AMPA receptors involve the activation of Nethylmaleimide-sensitive factor (NSF) and the subsequent recruitment of the AMPA receptor-associated PDZ scaffolding molecules (Narisawa-Saito et al, 2002;Jourdi et al, 2003). Our recent results indicate that EGF and other ErbB1 ligands down-regulates the expression of the AMPA receptor-associating PDZ molecules such as SAP-97 and GRIP, which bind to AMPA receptors and stabilize them by providing a link to cytoskeleton of postsynaptic sites (Yokomaku et al, 2005).…”

Section: Competition Between the Positive And Negative Regulators Bdmentioning

confidence: 97%

“…[ 3 H]AMPA binding assays were performed to test whether the down-regulation of GluR1 protein resulted in a change in AMPA receptor activity on the cell surface (Narisawa-Saito et al, 2002). After 4-day treatment with TGFα, various concentrations of [ 3 H]AMPA were applied to living cultures, and the cell surface binding of radioactive AMPA was measured in each dish.…”

Section: Tgfα Decreases Total Ampa Binding In Neocortical Culturementioning

confidence: 99%

“…We have previously shown multiple effects of BDNF in the regulation of AMPA receptors, including their protein expression, interaction with cytoskeletal components and partner PDZ proteins, and channel activity and localizations (Narisawa-Saito et al, 2002;Jourdi et al, 2003). In addition, BDNF effects on AMPA receptors involve the activation of Nethylmaleimide-sensitive factor (NSF) and the subsequent recruitment of the AMPA receptor-associated PDZ scaffolding molecules (Narisawa-Saito et al, 2002;Jourdi et al, 2003).…”

Section: Competition Between the Positive And Negative Regulators Bdmentioning

confidence: 99%

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Transforming growth factor alpha attenuates the functional expression of AMPA receptors in cortical GABAergic neurons

Namba

Nagano

Iwakura

et al. 2006

Molecular and Cellular Neuroscience

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In the developing neocortex, brain-derived neurotrophic factor (BDNF) exerts a trophic activity to increase the expression and channel activity of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptor subunits. Here, we demonstrate that the epidermal growth factor (EGF) receptor (ErbB1) ligands exert the opposite biological activity in cultured neocortical neurons. Subchronic stimulation of ErbB1 with transforming growth factor α (TGFα), EGF, or heparin-binding EGF (HB-EGF) down-regulated protein expression of the GluR1 AMPA receptor subunit in cultured neocortical neurons. In agreement, TGFα treatment decreased the B max of [ 3 H] AMPA binding and GluR1 mRNA levels. Immunocytochemistry revealed that the decrease in GluR1 was most pronounced in multipolar GABAergic neurons. To examine the physiological consequences, we recorded AMPA-evoked currents as well as miniature excitatory postsynaptic currents in morphologically identified putative GABAergic neurons in culture. Subchronic TGFα treatment decreased AMPA-triggered currents as well as the amplitude and frequency of miniature excitatory postsynaptic currents. An ErbB1 tyrosine kinase inhibitor, PD153035, inhibited the TGFα effect. Moreover, TGFα counteracted the neurotrophic activity of BDNF on AMPA receptor expression. Co-application of TGFα with BDNF blocked the BDNF-triggered up-regulation of AMPA receptor expression and currents. These observations reveal a negative regulatory activity of the ErbB1 ligand, TGFα, which reduces the input sensitivity of cortical GABAergic neurons to attenuate their inhibitory function.

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Section: Antagonistic Effects Of Tgfα Against Bdnfsupporting

confidence: 54%

Section: Competition Between the Positive And Negative Regulators Bdmentioning

confidence: 97%

Section: Tgfα Decreases Total Ampa Binding In Neocortical Culturementioning

confidence: 99%

Section: Competition Between the Positive And Negative Regulators Bdmentioning

confidence: 99%

See 2 more Smart Citations

Transforming growth factor alpha attenuates the functional expression of AMPA receptors in cortical GABAergic neurons

Namba

Nagano

Iwakura

et al. 2006

Molecular and Cellular Neuroscience

Self Cite

View full text Add to dashboard Cite

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“…Prolonged signaling by neurotrophins promotes quantal scaling of excitatory and inhibitory synapses in postnatal neural networks by modulating postsynaptic receptors (Rutherford et al, 1997;Rutherford et al, 1998). At glutamatergic synapses, BDNF promotes maturation of silent synapses by increasing the translocation of the GluR2 AMPA-receptor subunit to the neuronal surface in neocortical neurons (Narisawa-Saito et al, 1999;Narisawa-Saito et al, 2002). In hippocampal neurons, BDNF rapidly increases the phosphorylation and potentiates the conductance of NMDA receptors (Levine et al, 1996;Levine et al, 1998).…”

Section: Neurotrophins As Synaptic Modulators: Postsynaptic Neurotranmentioning

confidence: 99%

Neurotrophin signaling among neurons and glia during formation of tripartite synapses

Elmariah

Hughes

et al. 2004

Neuron Glia Biol.

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Synapse formation in the CNS is a complex process that involves the dynamic interplay of numerous signals exchanged between pre-and postsynaptic neurons as well as perisynaptic glia. Members of the neurotrophin family, which are widely expressed in the developing and mature CNS and are wellknown for their roles in promoting neuronal survival and differentiation, have emerged as key synaptic modulators. However, the mechanisms by which neurotrophins modulate synapse formation and function are poorly understood. Here, we summarize our work on the role of neurotrophins in synaptogenesis in the CNS, in particular the role of these signaling molecules and their receptors, the Trks, in the development of excitatory and inhibitory hippocampal synapses. We discuss our results that demonstrate that postsynaptic TrkB signaling plays an important role in modulating the formation and maintenance of NMDA and GABAA receptor clusters at central synapses, and suggest that neurotrophin signaling coordinately modulates these receptors as part of mechanism that promotes the balance between excitation and inhibition in developing circuits. We also discuss our results that demonstrate that astrocytes promote the formation of GABAergic synapses in vitro by differentially regulating the development of inhibitory presynaptic terminals and postsynaptic GABAA receptor clusters, and suggest that glial modulation of inhibitory synaptogenesis is mediated by neurotrophin-dependent and -independent signaling. Together, these findings extend our understanding of how neuron-glia communication modulates synapse formation, maintenance and function, and set the stage for defining the cellular and molecular mechanisms by which neurotrophins and other cell-cell signals direct synaptogenesis in the developing brain.

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From modulator to mediator: rapid effects of BDNF on ion channels

et al. 2004

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Neurotrophins (NTs) are [?AUTHOR] a family of structurally related, secreted proteins that regulate the survival, differentiation and maintenance of function of different populations of peripheral and central neurons.1,2 Among these, BDNF (brain-derived neurotrophic factor) has drawn considerable interest because both its synthesis and secretion are increased by physiological levels of activity, indicating a unique role of this neurotrophin in coupling neuronal activity to structural and functional properties of neuronal circuits. In addition to its classical neurotrophic effects, which are evident within hours or days and which usually result from changes in cellular gene expression, BDNF exerts acute effects on synaptic transmission and is involved in the induction of long-term potentiation. Many of these rapid effects of BDNF are mediated by its modulation of ion channel properties following TrkB-mediated activation of intracellular second messenger cascades and protein phosphorylation. However, recent reports have shown that BDNF not only acts as a modulator of ion channels, but can also directly and rapidly gate a Na(+) channel, thereby assigning BDNF the properties of a classical excitatory transmitter. Thus, BDNF, in addition its role as a potent neuromodulator, emerges as an excitatory transmitter-like substance which acutely controls resting membrane potential, neuronal excitability, synaptic transmission and participates in the induction of synaptic plasticity.

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Brain-derived Neurotrophic Factor Regulates Surface Expression of α-Amino-3-hydroxy-5-methyl-4-isoxazoleproprionic Acid Receptors by Enhancing the N-Ethylmaleimide-sensitive Factor/GluR2 Interaction in Developing Neocortical Neurons

Cited by 94 publications

References 57 publications

Transforming growth factor alpha attenuates the functional expression of AMPA receptors in cortical GABAergic neurons

Transforming growth factor alpha attenuates the functional expression of AMPA receptors in cortical GABAergic neurons

Neurotrophin signaling among neurons and glia during formation of tripartite synapses

From modulator to mediator: rapid effects of BDNF on ion channels

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