Ipsilateral versus contralateral spontaneous post-stroke neuroplastic changes: Involvement of BDNF?

Madinier, Alexandre; Bertrand, Nathalie; Rodier, Marion; Quirié, Aurore; Mossiat, Claude; Prigent‐Tessier, Anne; Marie, Christine; Garnier, Philippe

doi:10.1016/j.neuroscience.2012.11.054

Cited by 42 publications

(28 citation statements)

References 54 publications

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“…BDNF could promote the survival of new neurons arising from adult rats (Kirschenbaum and Goldman, 1995) and exert anti-apoptotic effects after ischemia (Guan et al, 2012). A delayed and sustained increase implies that ischemia-triggered BDNF expression may participate in post-stroke brain plasticity which may facilitate motor recovery (Madinier et al, 2013). This study also demonstrated that expression of BDNF increased significantly at 24 h and 48 h after ischemic reperfusion.…”

Section: Discussionsupporting

confidence: 55%

Over-expressed EGR1 may exaggerate ischemic injury after experimental stroke by decreasing BDNF expression

et al. 2015

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Section: Discussionsupporting

confidence: 55%

Over-expressed EGR1 may exaggerate ischemic injury after experimental stroke by decreasing BDNF expression

et al. 2015

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“…Proteins were separated on 10% (p-TrkB) or 12% (Pro-BDNF, FL-TrkB and mature BDNF) SDS–polyacrylamide gel electrophoresis (PAGE) and were electrophoretically transferred onto PVDF membrane (0.2 μm pore size) in cold transfer buffer [10 mM NaHCO 3 , 3 mM Na 2 CO 3 (pH 9.9) and 20% methanol]. Specificity of the different BDNF antibodies was characterized previously [25]. The membranes were incubated overnight at 4°C in 5% non-fat dry milk or 7.5% BSA (p-TrkB) in TBS [20 mM Tris–HCl (pH 7.6) and 137 mM NaCl] containing 0.1% Tween 20 to block unspecific binding.…”

Section: Methodsmentioning

confidence: 99%

Exogenous t-PA Administration Increases Hippocampal Mature BDNF Levels. Plasmin- or NMDA-Dependent Mechanism?

et al. 2014

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Brain-derived neurotrophic factor (BDNF) through TrkB activation is central for brain functioning. Since the demonstration that plasmin is able to process pro-BDNF to mature BDNF and that these two forms have opposite effects on neuronal survival and plasticity, a particular attention has been paid to the link between tissue plasminogen activator (tPA)/plasmin system and BDNF metabolism. However, t-PA via its action on different N-methyl-D-aspartate (NMDA) receptor subunits is also considered as a neuromodulator of glutamatergic transmission. In this context, the aim of our study was to investigate the effect of recombinant (r)t-PA administration on brain BDNF metabolism in rats. In the hippocampus, we found that rt-PA (10 mg/kg) administration induced a progressive increase in mature BDNF levels associated with TrkB activation. In order to delineate the mechanistic involved, plasmin activity was assessed and its inhibition was attempted using tranexamic acid (30 or 300 mg/kg, i.v.) while NMDA receptors were antagonized with MK801 (0.3 or 3 mg/kg, i.p.) in combination with rt-PA treatment. Our results showed that despite a rise in rt-PA activity, rt-PA administration failed to increase hippocampal plasmin activity suggesting that the plasminogen/plasmin system is not involved whereas MK801 abrogated the augmentation in mature BDNF levels observed after rt-PA administration. All together, our results show that rt-PA administration induces increase in hippocampal mature BDNF expression and suggests that rt-PA contributes to the control of brain BDNF synthesis through a plasmin-independent potentiation of NMDA receptors signaling.

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“…In animal models of ischemic stroke, a permanent BDNF reduction has been observed in the infarct core, while rapid upregulation of neurotrophin expression lasting for several days was found in the penumbra [25,26]. However, BDNF has never been measured in the postmortem brains of stroke patients, although a slight increase in circulating neurotrophin levels observed after stroke could mirror brain levels [27].…”

Section: Defective Expression and Stability Of Bdnf And Trkb In Nementioning

confidence: 99%

Integral Characterization of Defective BDNF/TrkB Signalling in Neurological and Psychiatric Disorders Leads the Way to New Therapies

Tejeda

Dı́az-Guerra

2017

IJMS

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Enhancement of brain-derived neurotrophic factor (BDNF) signalling has great potential in therapy for neurological and psychiatric disorders. This neurotrophin not only attenuates cell death but also promotes neuronal plasticity and function. However, an important challenge to this approach is the persistence of aberrant neurotrophic signalling due to a defective function of the BDNF high-affinity receptor, tropomyosin-related kinase B (TrkB), or downstream effectors. Such changes have been already described in several disorders, but their importance as pathological mechanisms has been frequently underestimated. This review highlights the relevance of an integrative characterization of aberrant BDNF/TrkB pathways for the rational design of therapies that by combining BDNF and TrkB targets could efficiently promote neurotrophic signalling.

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Ipsilateral versus contralateral spontaneous post-stroke neuroplastic changes: Involvement of BDNF?

Cited by 42 publications

References 54 publications

Over-expressed EGR1 may exaggerate ischemic injury after experimental stroke by decreasing BDNF expression

Over-expressed EGR1 may exaggerate ischemic injury after experimental stroke by decreasing BDNF expression

Exogenous t-PA Administration Increases Hippocampal Mature BDNF Levels. Plasmin- or NMDA-Dependent Mechanism?

Integral Characterization of Defective BDNF/TrkB Signalling in Neurological and Psychiatric Disorders Leads the Way to New Therapies

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