Brain-derived neurotrophic factor rapidly potentiates synaptic transmission through NMDA, but suppresses it through non-NMDA receptors in rat hippocampal neuron

Song, Dae‐Kyu; Choe, B. K.; Bae, Jae Hoon; Park, Won Kyun; Han, In Sook; Ho, Won‐Kyung; Earm, Yung E.

doi:10.1016/s0006-8993(98)00474-0

Cited by 41 publications

(21 citation statements)

References 27 publications

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“…Moreover, BDNF increased the amplitude of EPSCs in the presence of the non-NMDA receptor antagonist CNQX, and the response to iontophoretically applied NMDA, but not AMPA or acetylcholine. These results suggest that NMDA receptor responses are selectively enhanced by BDNF Song et al, 1998). Consistent with this finding, TrkB is localized to the postsynaptic density (Wu et al, 1996), and activation of the TrkB receptor leads to phosphorylation of the NMDA receptor subunits I and 2B Suen et al, 1998).…”

Section: Postsynaptic Modulatory Effectsupporting

confidence: 71%

Neurotrophins and hippocampal synaptic transmission and plasticity

Chow

1999

J. Neurosci. Res.

233

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Neurotrophins are traditionally thought to be secretory proteins that regulate long-term survival and differentiation of neurons. Recent studies have revealed a previously unexpected role for neurotrophins in synaptic development and plasticity in diverse neuronal populations. In this review, we focus on the synaptic function of brain-derived neurotrophic factor (BDNF) in the hippocampus. Although a variety of in vitro experiments have shown the ability of BDNF to acutely modulate synaptic transmission, whether BDNF truly potentiates basal synaptic transmission in hippocampal neurons remains controversial. More consistent evidence has been obtained for the role of BDNF in long-term potentiation (LTP), a cellular model for learning and memory. BDNF also potentiates high frequency transmission by modulating the number of docked vesicles and the levels of the vesicle protein synaptobrevin and synaptophysin at the CA1 synapses. Both pre- and postsynaptic effects of BDNF have been demonstrated. Recent studies have begun to address the role of BDNF in late-phase LTP and in the development of hippocampal circuit. BDNF and other neurotrophins may represent a new class of neuromodulators that regulate neuronal connectivity and synaptic efficacy. J. Neurosci. Res. 58:76-87, 1999. Published 1999 Wiley-Liss, Inc.

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Section: Postsynaptic Modulatory Effectsupporting

confidence: 71%

Neurotrophins and hippocampal synaptic transmission and plasticity

Chow

1999

J. Neurosci. Res.

233

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“…With respect to NMDA receptor subunit involvement in learning and memory, restricted genetic deletion of the NR1 subunit in the CA1 region of the hippocampus using the conditional Cre/loxP recombination approach produces impaired NMDA-dependent LTP, and spatial memory (Tsien et al 1996a,b). It was subsequently reported that BDNF increases NMDA-mediated currents, as well as the NMDA receptor component of evoked EPSCs in cultured hippocampal neurons (Sakai et al 1997;Levine et al 1998;Song et al 1998;Crozier et al 1999). Specifically, single-channel analysis indicated that BDNF rapidly increased the single-channel open probability (P o ) of NMDA receptors, but did not affect the mean open time or unitary conductance in outside-out patch (Jarvis et al 1997) or cellattached ) recordings in cultured hippocampal neurons.…”

Section: Bdnf and Memory Consolidationmentioning

confidence: 98%

From Acquisition to Consolidation: On the Role of Brain-Derived Neurotrophic Factor Signaling in Hippocampal-Dependent Learning

Tyler¹,

Alonso²,

Bramham³

et al. 2002

Learn. Mem.

627

398

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One of the most rigorously investigated problems in modern neuroscience is to decipher the mechanisms by which experience-induced changes in the central nervous system are translated into behavioral acquisition, consolidation, retention, and subsequent recall of information. Brain-derived neurotrophic factor (BDNF) has recently emerged as one of the most potent molecular mediators of not only central synaptic plasticity, but also behavioral interactions between an organism and its environment. Recent experimental evidence indicates that BDNF modulates synaptic transmission and plasticity by acting across different spatial and temporal domains. BDNF signaling evokes both short-and long-term periods of enhanced synaptic physiology in both pre-and postsynaptic compartments of central synapses. Specifically, BDNF/TrkB signaling converges on the MAP kinase pathway to enhance excitatory synaptic transmission in vivo, as well as hippocampal-dependent learning in behaving animals. Emerging concepts of the intracellular signaling cascades involved in synaptic plasticity induced through environmental interactions resulting in behavioral learning further support the contention that BDNF/TrkB signaling plays a fundamental role in mediating enduring changes in central synaptic structure and function. Here we review recent literature showing the involvement of BDNF/TrkB signaling in hippocampal-dependent learning paradigms, as well as in the types of cellular plasticity proposed to underlie learning and memory.

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“…5). Although the exact relationship is unknown, BDNF has been demonstrated to potentiate synaptic transmission through the NMDA-R (Song et al, 1998). Furthermore, BDNF through its TrkB-R (Jovanovic et al, 1996), and the NMDA-R through CAMKII (Platenik et al, 2000), can both converge on MAP-K.…”

Section: The Role Of Map-k: Modulation Of Creb Mrna Levelsmentioning

confidence: 99%

Interplay between brain-derived neurotrophic factor and signal transduction modulators in the regulation of the effects of exercise on synaptic-plasticity

Vaynman¹,

Ying²,

2003

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Abstract-This study was designed to identify molecular mechanisms by which exercise affects synaptic-plasticity in the hippocampus, a brain area whose function, learning and memory, depends on this capability. We have focused on the central role that brain-derived neurotrophic factor (BDNF) may play in mediating the effects of exercise on synapticplasticity. In fact, this impact of exercise is exemplified by our finding that BDNF regulates the mRNA levels of two end products important for neural function, i.e. cAMP-responseelement binding (CREB) protein and synapsin I. CREB and synapsin I have the ability to modify neuronal function by regulating gene-transcription and affecting synaptic transmission, respectively. Furthermore, we show that BDNF is capable of concurrently increasing the mRNA levels of both itself and its tyrosine kinaseB (TrkB) receptor, suggesting that exercise may employ a feedback loop to augment the effects of BDNF on synaptic-plasticity. The use of a novel microbead injection method in our blocking experiments and Taqman reverse transcription polymerase reaction (RT-PCR) for RNA quantification, have enabled us to evaluate the contribution of different pathways to the exercise-induced increases in the mRNA levels of BDNF, TrkB, CREB, and synapsin I. We found that although BDNF mediates exerciseinduced hippocampal plasticity, additional molecules, i.e. the N-methyl-D-aspartate receptor, calcium/calmodulin protein kinase II and the mitogen-activated protein kinase cascade, modulate its effects. Since these molecules have a well-described association to BDNF action, our results illustrate a basic mechanism through which exercise may promote synaptic-plasticity in the adult brain.

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Brain-derived neurotrophic factor rapidly potentiates synaptic transmission through NMDA, but suppresses it through non-NMDA receptors in rat hippocampal neuron

Cited by 41 publications

References 27 publications

Neurotrophins and hippocampal synaptic transmission and plasticity

Neurotrophins and hippocampal synaptic transmission and plasticity

From Acquisition to Consolidation: On the Role of Brain-Derived Neurotrophic Factor Signaling in Hippocampal-Dependent Learning

Interplay between brain-derived neurotrophic factor and signal transduction modulators in the regulation of the effects of exercise on synaptic-plasticity

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