Postsynaptic Induction of BDNF-Mediated Long-Term Potentiation

Kovalchuk, Yury; Hanse, Eric; Kafitz, Karl W.; Konnerth, Arthur

doi:10.1126/science.1067766

Cited by 429 publications

(272 citation statements)

References 38 publications

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“…However, in this study no experiments were performed to analyze the response in mice lacking presynaptic TrkB receptors and therefore the authors concluded that BDNF would target presynaptic TrkB receptors to induce synaptic potentiation. In contrast with the reports suggesting a concurrent role of pre-and post-synaptic TrkB receptors in LTP in the CA1 region of the hippocampus, a postsynaptic effect was proposed to account for the robust induction of LTP at the synapses of the medial perforant path fibers when BDNF was applied together with a weak synaptic stimulation that would not normally induce synaptic potentiation (Kovalchuk et al, 2002). Although a presynaptic effect of BDNF was not ruled out in this paradigm, the differences may be due to the distinct synapses investigated.…”

Section: Bdnf and Ltp In The Hippocampusmentioning

confidence: 47%

“…Facilitatory effects of BDNF in the induction of LTP have also been reported under conditions of weak synaptic stimulation that would not normally induce synaptic potentiation in the hippocampal CA1 region (Kovalchuk et al, 2002). Bath application of BDNF also triggers a sustained enhancement of synaptic transmission in the CA1 region of the hippocampus by a mechanism dependent on protein synthesis (Ji et al, 2010;Kang and Schuman, 1996).…”

Section: Bdnf and Ltp In The Hippocampusmentioning

confidence: 91%

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BDNF-induced local protein synthesis and synaptic plasticity

2014

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a b s t r a c tBrain-derived neurotrophic factor (BDNF) is an important regulator of synaptic transmission and longterm potentiation (LTP) in the hippocampus and in other brain regions, playing a role in the formation of certain forms of memory. The effects of BDNF in LTP are mediated by TrkB (tropomyosin-related kinase B) receptors, which are known to be coupled to the activation of the Ras/ERK, phosphatidylinositol 3-kinase/Akt and phospholipase C-g (PLC-g) pathways. The role of BDNF in LTP is best studied in the hippocampus, where the neurotrophin acts at pre-and post-synaptic levels. Recent studies have shown that BDNF regulates the transport of mRNAs along dendrites and their translation at the synapse, by modulating the initiation and elongation phases of protein synthesis, and by acting on specific miRNAs. Furthermore, the effect of BDNF on transcription regulation may further contribute to long-term changes in the synaptic proteome. In this review we discuss the recent progress in understanding the mechanisms contributing to the short-and long-term regulation of the synaptic proteome by BDNF, and the role in synaptic plasticity, which is likely to influence learning and memory formation.This article is part of the Special Issue entitled 'BDNF Regulation of Synaptic Structure, Function, and Plasticity'.

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Section: Bdnf and Ltp In The Hippocampusmentioning

confidence: 47%

Section: Bdnf and Ltp In The Hippocampusmentioning

confidence: 91%

BDNF-induced local protein synthesis and synaptic plasticity

2014

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“…Additional findings that high-frequency stimulation or more natural theta patterns of afferent activity upregulates BDNF expression further corroborate its role in synaptic plasticity (Gooney and Lynch, 2001;Balkowiec and Katz, 2002). Mechanisms underlying the function of BDNF in plasticity include presynaptic (Gottschalk et al, 1998;Pozzo-Miller et al, 1999;Jovanovic et al, 2000;Xu et al, 2000;Zakharenko et al, 2003;Tyler et al, 2006) or postsynaptic actions Lin et al, 1998;Di Luca et al, 2001;Kovalchuk et al, 2002) as well as coordinate pre-and postsynaptic processes (Alder et al, 2005;Gartner et al, 2006). Despite a great deal of progress on the function of BDNF in LTP, investigation of its role in associative learning has only more recently begun to be examined.…”

Section: Introductionmentioning

confidence: 62%

“…The deficits in LTP resulting from BDNF knockdown could be rescued by addition of recombinant BDNF to medium (Patterson et al, 1996) or adenovirus-mediated overexpression of BDNF (Korte et al, 1996). Studies have also suggested that BDNF itself could induce (Messaoudi et al, 1998) or facilitate (Kovalchuk et al, 2002) LTP expression in the hippocampus. Additional findings that high-frequency stimulation or more natural theta patterns of afferent activity upregulates BDNF expression further corroborate its role in synaptic plasticity (Gooney and Lynch, 2001;Balkowiec and Katz, 2002).…”

Section: Introductionmentioning

confidence: 87%

Coordinate action of pre- and postsynaptic brain-derived neurotrophic factor is required for AMPAR trafficking and acquisition of in vitro classical conditioning

Keifer

2008

Neuroscience

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Brain-derived neurotrophic factor (BDNF) has been implicated in mechanisms of synaptic plasticity such as long-term potentiation (LTP), but its role in associative learning remains largely unknown. In the present study, we investigated the function of BDNF and its receptor tropomyosin-related kinase B (TrkB) in an in vitro model of classical conditioning. Conditioning resulted in a significant increase in BDNF and phospho (p)-Trk expression. Bath application of antibodies directed against TrkB, but not TrkA or TrkC, abolished acquisition of conditioning, as did a receptor tyrosine kinase inhibitor K252a and an inhibitor of nitric oxide synthase 7-nitroindazole. Significantly, injections of BDNF Ab into the nerve roots of presynaptic axonal projections or postsynaptic motor neurons prevented acquisition of conditioning, suggesting that BDNF is required on both sides of the synapse for modification to occur. The presynaptic proteins synaptophysin and synapsin I were increased upon conditioning or BDNF application. Furthermore, BDNF application alone mimicked conditioning-induced synaptic insertion of GluR1 and GluR4 AMPAR subunits into synapses, which was inhibited by co-application of BDNF and K252a. Data also show that extracellular signalregulated kinase (ERK) was activated in BDNF-treated preparations. We conclude that coordinate pre-and postsynaptic actions of BDNF are required for acquisition of in vitro classical conditioning.

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“…A subcellular fractionation procedure was used to separate protein from the cytosolic and synaptic membrane compartments because there can also be local synthesis of BDNF in dendrites (Hartmann et al, 2001;Kovalchuk et al, 2002), where it can directly affect synaptic plasticity. Tissue was homogenized in a Tris buffer containing a cocktail of protease inhibitors (Sacktor et al, 1993).…”

Section: Hippocampal Protein Isolationmentioning

confidence: 99%

Prenatal opiate exposure impairs radial arm maze performance and reduces levels of BDNF precursor following training

2008

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Prenatal exposure to opiates, which is invariably followed by postnatal withdrawal, can affect cognitive performance. To further characterize these effects, we examined radial 8-arm maze performance and expression of brain derived neurotrophic factor (BDNF) in male rats prenatally exposed to the opiate l-α-acetylmethadol (LAAM). Female rats received 1.0 mg/kg/day LAAM or water via daily oral gavage for 28 days prior to breeding, during breeding, and throughout pregnancy. Pups were fostered to non-treated lactating dams at birth and underwent neonatal opiate withdrawal. At 5-6 months, prenatal water-and LAAM-exposed males (n=6 each; non-littermates) received radial arm maze training consisting of ten trials a day for five days and three retention trials on day six. Rats prenatally exposed to LAAM had poorer maze performance, decreased percent correct responding and more reference and working memory errors than prenatal water-treated controls. However, they were able to acquire the task by the end of training. There were no differences between the groups on retention 24 hr after testing. Following retention testing, hippocampi were removed and protein extracted from cytosol and synaptic fractions. Western blots were used to measure levels of mature and precursor BDNF protein, as well as the BDNF receptor TrkB. BDNF precursor protein was significantly decreased in the synaptic fraction of trained prenatal LAAM-treated rats compared to prenatal water-treated trained controls. No effects were found for the full-length or truncated TrkB receptor. In untrained rats, prenatal treatment did not affect any of the measures. These data suggest that prenatal opiate exposure and/or postnatal withdrawal compromise expression of proteins involved in the neural plasticity underlying learning.

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Postsynaptic Induction of BDNF-Mediated Long-Term Potentiation

Cited by 429 publications

References 38 publications

BDNF-induced local protein synthesis and synaptic plasticity

BDNF-induced local protein synthesis and synaptic plasticity

Coordinate action of pre- and postsynaptic brain-derived neurotrophic factor is required for AMPAR trafficking and acquisition of in vitro classical conditioning

Prenatal opiate exposure impairs radial arm maze performance and reduces levels of BDNF precursor following training

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