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

Rose, Christine R.; Blum, Robert; Kafitz, Karl W.; Kovalchuk, Yury; Konnerth, Arthur

doi:10.1002/bies.20118

Cited by 107 publications

(90 citation statements)

References 89 publications

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“…BDNF is also known www.chinaphar.com Xie H et al Acta Pharmacologica Sinica npg to be expressed and released in an activity-dependent manner in the central nervous system and can acutely modulate synaptic transmission and plasticity [40][41][42][43] . In a previous study, we and co-workers reported that BDNF is critical in the expression of L-LTP in the hippocampus suggesting that it is a key protein in long-term memory formation [44] .…”

Section: Critical Role Of Decreased Bdnf Expression In Chronic Intermmentioning

confidence: 99%

Chronic intermittent hypoxia-induced deficits in synaptic plasticity and neurocognitive functions: a role for brain-derived neurotrophic factor

Xie

Yung

2012

Acta Pharmacol Sin

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Obstructive sleep apnea (OSA) is well known for its metabolic as well as neurobehavioral consequences. Chronic intermittent hypoxia (IH) is a major component of OSA. In recent years, substantial advances have been made in elucidating the cellular and molecular mechanisms underlying the effect of chronic IH on neurocognitive functions, many of which are based on studies in animal models. A number of hypotheses have been put forward to explain chronic IH-induced neurological dysfunctions. Among these, the roles of oxidative stress and apoptosis-related neural injury are widely accepted. Here, focusing on results derived from animal studies, we highlight a possible role of reduced expression of brain-derived neurotrophic factor (BDNF) in causing impairment in long-term synaptic plasticity and neurocognitive functions during chronic IH. The possible relationship between BDNF and previous findings on this subject will be elucidated.

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Section: Critical Role Of Decreased Bdnf Expression In Chronic Intermmentioning

confidence: 99%

Chronic intermittent hypoxia-induced deficits in synaptic plasticity and neurocognitive functions: a role for brain-derived neurotrophic factor

Xie

Yung

2012

Acta Pharmacol Sin

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“…Akt signalling regulates the translation and transport of synaptic proteins in order to promote synaptic plasticity in learning and memory (Yoshii and Constantine-Paton, 2007). Along with the activation of TrkB, BDNF also triggers the opening of Na + gated ion channels, resulting in an influx of Ca 2+ and the enhancement of glutamate activation of N-methyl-D-aspartate (NMDA) receptors (Rose et al , 2004). NMDA receptors also play a crucial role in synaptic plasticity with their activation by glutamate leading to the induction of LTP Collingridge, 1993, Cooke andBliss, 2006).…”

Section: Introductionmentioning

confidence: 99%

Bardoxolone methyl prevents high-fat diet-induced alterations in prefrontal cortex signalling molecules involved in recognition memory

Camer

Szabo

et al. 2015

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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X. (2015). Bardoxolone methyl prevents high-fat diet-induced alterations in prefrontal cortex signalling molecules involved in recognition memory. Progress in Neuro-Psychopharmacology and Biological Psychiatry, 59 68-75. Bardoxolone methyl prevents high-fat diet-induced alterations in prefrontal cortex signalling molecules involved in recognition memory AbstractHigh fat (HF) diets are known to induce changes in synaptic plasticity in the forebrain leading to learning and memory impairments. Previous studies of oleanolic acid derivatives have found that these compounds can cross the blood-brain barrier to prevent neuronal cell death. We examined the hypothesis that the oleanolic acid derivative, bardoxolone methyl (BM) would prevent diet-induced cognitive deficits in mice fed a HF diet. C57BL/6J male mice were fed a lab chow (LC) (5% of energy as fat), a HF (40% of energy as fat), or a HF diet supplemented with 10 mg/kg/day BM orally for 21 weeks. Recognition memory was assessed by performing a novel object recognition test on the treated mice. Downstream brain-derived neurotrophic factor (BDNF) signalling molecules were examined in the prefrontal cortex (PFC) and hippocampus of mice via Western blotting and N-methyl-d-aspartate (NMDA) receptor binding. BM treatment prevented HF dietinduced impairment in recognition memory (p < 0.001). In HF diet fed mice, BM administration attenuated alterations in the NMDA receptor binding density in the PFC (p < 0.05), however, no changes were seen in the hippocampus (p > 0.05). In the PFC and hippocampus of the HF diet fed mice, BM administration improved downstream BDNF signalling as indicated by increased protein levels of BDNF, phosphorylated tropomyosin related kinase B (pTrkB) and phosphorylated protein kinase B (pAkt), and increased phosphorylated AMP-activated protein kinase (pAMPK) (p < 0.05). BM administration also prevented the HF diet-induced increase in the protein levels of inflammatory molecules, phosphorylated c-Jun N-terminal kinase (pJNK) in the PFC, and protein tyrosine phosphatase 1B (PTP1B) in both the PFC and hippocampus. In summary, these findings suggest that BM prevents HF diet-induced impairments in recognition memory by improving downstream BDNF signal transduction, increasing pAMPK, and reducing inflammation in the PFC and hippocampus. AbstractHigh-fat (HF) diets are known to induce changes in synaptic plasticity in the forebrain leading to learning and memory impairments. Previous studies of oleanolic acid derivatives have found that these compounds can cross the blood brain barrier to prevent neuronal cell death. We examined the hypothesis that the oleanolic acid derivative, bardoxolone methyl (BM) would prevent diet-induced cognitive deficits in mice fed a HF diet. C57BL/6J male mice were fed a lab chow (LC) (5% of energy as fat), HF (40% of energy as fat), or HF diet supplemented with 10 mg/kg/day BM orally for 21 weeks. and phosphorylated protein kinase B (pAkt), and increased phosphorylated AMP-activated protein kinase (pAMPK) (p<0.05). BM a...

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“…Tropomyosin receptor kinase B (TrkB, also known as NTRK2), as the high-affinity receptor for BDNF, are abundant in the nervous system and are crucial for synaptic plasticity in the CNS (Bramham and Messaoudi, 2005;Nagappan and Lu, 2005;Cohen and Greenberg, 2008). When activated by BDNF, TrkB receptors initiate three major signaling cascades, including those mediated by phosphoinositide 3-kinase (PI3K), phospholipase Cc (PLCc) and extracellular signal-regulated kinase 1 and 2 (ERK1/2; also known as MAPK3 and MAPK1, respectively) (Huang and Reichardt, 2003;Segal, 2003), thereby regulating synaptic transmission and membrane excitability in neurons (Poo, 2001;Rose et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Myosin5a mediates BDNF-induced postendocytic recycling of full-length TrkB and its translocation into dendritic spines

Sui

Huang

Wang

et al. 2015

Journal of Cell Science

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Brain-derived neurotrophic factor (BDNF) plays an important role in neuronal survival, neurite outgrowth and synaptic plasticity by activating the receptor tropomyosin receptor kinase B (TrkB, also known as NTRK2). TrkB has been shown to undergo recycling after BDNF stimulation. We have previously reported that full-length TrkB (TrkB-FL) are recycled through a Rab11-dependent pathway upon BDNF stimuli, which is important for the translocation of TrkB-FL into dendritic spines and for the maintenance of prolonged BDNF downstream signaling during long-term potentiation (LTP). However, the identity of the motor protein that mediates the local transfer of recycled TrkB-FL back to the plasma membrane remains unclear. Here, we report that the F-actin-based motor protein myosin Va (Myo5a) mediates the postendocytic recycling of TrkB-FL. Blocking the interaction between Rab11 and Myo5a by use of a TAT-tagged peptide consisting of amino acids 55-66 of the Myo5a ExonE domain weakened the association between TrkB-FL and Myo5a and thus impaired TrkB-FL recycling and BDNF-induced TrkB-FL translocation into dendritic spines. Finally, inhibiting Myo5a-mediated TrkB-FL recycling led to a significant reduction in prolonged BDNF downstream signaling. Taken together, these results show that Myo5a mediates BDNF-dependent TrkB-FL recycling and contributes to BDNF-induced TrkB spine translocation and prolonged downstream signaling.

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

Cited by 107 publications

References 89 publications

Chronic intermittent hypoxia-induced deficits in synaptic plasticity and neurocognitive functions: a role for brain-derived neurotrophic factor

Chronic intermittent hypoxia-induced deficits in synaptic plasticity and neurocognitive functions: a role for brain-derived neurotrophic factor

Bardoxolone methyl prevents high-fat diet-induced alterations in prefrontal cortex signalling molecules involved in recognition memory

Myosin5a mediates BDNF-induced postendocytic recycling of full-length TrkB and its translocation into dendritic spines

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