Status epilepticus induces a TrkB to p75 neurotrophin receptor switch and increases brain-derived neurotrophic factor interaction with p75 neurotrophin receptor: An initial event in neuronal injury induction

Unsain, Nicolás; Núñez, Nomelí P.; Anastasía, Agustín; Mascó, Daniel H.

doi:10.1016/j.neuroscience.2008.04.038

Cited by 50 publications

(63 citation statements)

References 94 publications

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“…This finding agrees with a previous report showing that levels of mature BDNF increased after status epilepticus in rats, whereas pro-BDNF levels did not change until 72 h after status epilepticus (Unsain et al, 2008). Importantly, (Ϫ/Ϫ) mice showed reduced levels of mature BDNF during the early stage of kindling, which may explain slower kindling development in the mutant animals.…”

Section: Discussionsupporting

confidence: 92%

Matrix Metalloproteinase-9 Contributes to Kindled Seizure Development in Pentylenetetrazole-Treated Mice by Converting Pro-BDNF to Mature BDNF in the Hippocampus

Mizoguchi¹,

Nakade²,

Terabe³

et al. 2011

J. Neurosci.

174

142

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(Ϫ/Ϫ) mice compared with wild-type mice, an observation that was accompanied by decreased hippocampal levels of mature brain-derived neurotrophic factor. Microinjecting the BDNF scavenger TrkB-Fc into the right ventricle before each PTZ treatment significantly suppressed the development of kindling in wild-type mice, whereas no effect was observed in MMP-9 (Ϫ/Ϫ) mice. On the other hand, bilateral injections of pro-BDNF into the hippocampal dentate gyrus significantly enhanced kindling in wild-type mice but not MMP-9 (Ϫ/Ϫ) mice. These findings suggest that MMP-9 is involved in the progression of behavioral phenotypes in kindled mice because of conversion of pro-BDNF to mature BDNF in the hippocampus.

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Section: Discussionsupporting

confidence: 92%

Matrix Metalloproteinase-9 Contributes to Kindled Seizure Development in Pentylenetetrazole-Treated Mice by Converting Pro-BDNF to Mature BDNF in the Hippocampus

Mizoguchi¹,

Nakade²,

Terabe³

et al. 2011

J. Neurosci.

174

142

View full text Add to dashboard Cite

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“…Neurotrophic factors have been suggested as possible therapeutic agents (for a review see Acharya et al 2008), but preclinical, basic research studies have shown that the classical neurotrophins NGF (Adams et al 1997;Li et al 2005) and BDNF (Binder et al 2001;Lähteinen et al 2002;Unsain et al 2008) have further damaging effects. In contrast, GDNF (Kanter-Schlifke et al 2007;Martin et al 1995), betaFGF (Liu et al 1993) and VEGF (Croll et al 2004) have been shown to be neuroprotective in the TLE animal model of kainic acid-induced hippocampal degeneration.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of IGF-I Following Kainic Acid-Induced Hippocampal Degeneration in the Rat

2009

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Insulin-like growth factor I (IGF-I) has been shown to act as a neuroprotectant both in in vitro studies and in in vivo animal models of ischemia, hypoxia, trauma in the brain or the spinal cord, multiple and amyotrophic lateral sclerosis, Alzheimer's and Parkinson's disease. In the present study, we investigated the neuroprotective potential of IGF-I in the "kainic acid-induced degeneration of the hippocampus" model of temporal lobe epilepsy. Increased cell death--as detected by FluoroJade B staining--and extensive cell loss--as determined by cresyl violet staining--were observed mainly in the CA3 and CA4 areas of the ipsilateral and contralateral hippocampus, 7 days following intrahippocampal administration of kainic acid. Kainic acid injection also resulted in intense astrogliosis--as assessed by the number of glial fibrillary acidic protein (GFAP) immunopositive cells--in both hemispheres, forming a clear astroglial scar ipsilaterally to the injection site. Heat-shock protein 70 (Hsp70) immunopositive cells were also observed in the ipsilateral dentate gyrus (DG) following kainic acid injection. When IGF-I was administered together with kainic acid, practically no signs of degeneration were detected in the contralateral hemisphere, while in the ipsilateral, there was a smaller degree of cell loss, reduced number of FluoroJade B-stained cells, decreased reactive gliosis and fewer Hsp70-positive cells. Our present results extend further the cases in which IGF-I is shown to exhibit neuroprotective properties in neurodegenerative processes in the CNS.

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“…In vitro studies demonstrate that BDNF provides neuroprotection during hypoglycemia by binding to the full-length isoform of TrkB (TrkB FL ) receptor and stabilizing calcium homeostasis (21,22). Conversely, binding of BDNF to p75 NTR receptor promotes neuronal injury (23,24). In the second experiment, we determined the neuroprotective efficacy of ketonemia by comparing the severity of neuronal injury in rats treated with β-hydroxybutyrate during hypoglycemia with those conventionally treated using 10% dextrose.…”

Section: Articlesmentioning

confidence: 99%

Hyperglycemia accentuates and ketonemia attenuates hypoglycemia-induced neuronal injury in the developing rat brain

et al. 2014

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Background: Prolonged hypoglycemia leads to brain injury, despite treatment with 10% dextrose. Whether induction of hyperglycemia or ketonemia achieves better neuroprotection is unknown. Hyperglycemia is neuroprotective in other brain injuries during development; however, it worsens hypoglycemia-induced injury in the adult brain via poly(ADPribose)polymerase-1 (PARP-1) overactivation. Methods: Three-week-old rats were subjected to insulininduced hypoglycemia and treated with 10% dextrose or 50% dextrose. Neuronal injury, PARP-1, and brain-derived neurotrophic factor (BDNF) III/TrkB/p75 NTR expressions were determined. In the second experiment, ketonemia was induced by administering β-hydroxybutyrate during hypoglycemia and its effect on neuronal injury was compared with those conventionally treated using 10% dextrose. results: Both 10 and 50% dextrose administration led to hyperglycemia (50% dextrose > 10% dextrose). Compared with the 10% dextrose group, neuronal injury was greater in the 50% dextrose group and was accompanied by PARP-1 overactivation. BDNF III and p75 NTR , but not TrkB FL , mRNA expressions were upregulated. Neuronal injury was less severe in the rats subjected to ketonemia, compared with those conventionally treated using 10% dextrose. conclusion: Hyperglycemia accentuated hypoglycemiainduced neuronal injury, likely via PARP-1 overactivation. Although BDNF was upregulated, it was not neuroprotective and potentially exaggerated injury by binding to p75 NTR receptor. Conversely, ketonemia during hypoglycemia attenuated neuronal injury.

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Status epilepticus induces a TrkB to p75 neurotrophin receptor switch and increases brain-derived neurotrophic factor interaction with p75 neurotrophin receptor: An initial event in neuronal injury induction

Cited by 50 publications

References 94 publications

Matrix Metalloproteinase-9 Contributes to Kindled Seizure Development in Pentylenetetrazole-Treated Mice by Converting Pro-BDNF to Mature BDNF in the Hippocampus

Matrix Metalloproteinase-9 Contributes to Kindled Seizure Development in Pentylenetetrazole-Treated Mice by Converting Pro-BDNF to Mature BDNF in the Hippocampus

Neuroprotective Effects of IGF-I Following Kainic Acid-Induced Hippocampal Degeneration in the Rat

Hyperglycemia accentuates and ketonemia attenuates hypoglycemia-induced neuronal injury in the developing rat brain

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