ArticleASN neuro2014
p75NTR, but not proNGF, is upregulated following status epilepticus in mice.
Article in ASN neuro, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Pentylenetetrazole kindling impairs place recognition memory associated with suppressing proBDNF-mediated neural information flows at the hippocampal CA3-CA1 synapses.Frontiers in pharmacology · 2026Article
- The functional and molecular roles of p75 neurotrophin receptor (p75Journal of central nervous system disease · 2024Review
- Relationship between chronic hypoxia and seizure susceptibility.CNS neuroscience & therapeutics · 2022Review
- Electroacupuncture treatment improves motor function and neurological outcomes after cerebral ischemia/reperfusion injury.Neural regeneration research · 2022Article
- Robust chronic convulsive seizures, high frequency oscillations, and human seizure onset patterns in an intrahippocampal kainic acid model in mice.Neurobiology of disease · 2022Article
- Neuronal apoptosis induced by morphine withdrawal is mediated by the p75 neurotrophin receptor.Journal of neurochemistry · 2021Article
- Up-regulation of the p75 neurotrophin receptor is an essential mechanism for HIV-gp120 mediated synaptic loss in the striatum.Brain, behavior, and immunity · 2020Article
- Effects of Cerebrolysin on Hippocampal Neuronal Death After Pilocarpine-Induced Seizure.Frontiers in neuroscience · 2020Article
- An Excitatory and Epileptogenic Effect of Dentate Gyrus Mossy Cells in a Mouse Model of Epilepsy.Cell reports · 2019Article
- Regulation of BACE1 expression after injury is linked to the p75 neurotrophin receptor.Molecular and cellular neurosciences · 2019Article
- Evidence for a non-canonical JAK/STAT signaling pathway in the synthesis of the brain's major ion channels and neurotransmitter receptors.BMC genomics · 2019Article
- Sex-Dependent Signaling Pathways Underlying Seizure Susceptibility and the Role of Chloride Cotransporters.Cells · 2019Review
- SorCS2 Controls Functional Expression of Amino Acid Transporter EAAT3 and Protects Neurons from Oxidative Stress and Epilepsy-Induced Pathology.Cell reports · 2019Article
- Loss of TrkB Signaling Due to Status Epilepticus Induces a proBDNF-Dependent Cell Death.Frontiers in cellular neuroscience · 2019Article
- Risk Locus Identification Ties Alcohol Withdrawal Symptoms to SORCS2.Alcoholism, clinical and experimental research · 2018Article
- Trkb-IP3 Pathway Mediating Neuroprotection in Rat Hippocampal Neuronal Cell Culture Following Induction of Kainic Acid.The Malaysian journal of medical sciences : MJMS · 2018Article
- Blockade of p75 Neurotrophin Receptor Reverses Irritability and Anxiety-Related Behaviors in a Rat Model of Status EpilepticusIranian biomedical journal · 2018Article
- PROneurotrophins and CONSequences.Molecular neurobiology · 2018Review
- Disruption of SorCS2 reveals differences in the regulation of stereociliary bundle formation between hair cell types in the inner ear.PLoS genetics · 2017Article
- Death Domain Signaling by Disulfide-Linked Dimers of the p75 Neurotrophin Receptor Mediates Neuronal Death in the CNS.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
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7 authors.
Funding
Abstract
ProNGF and p75(NTR) are upregulated and induce cell death following status epilepticus (SE) in rats. However, less is known about the proneurotrophin response to SE in mice, a more genetically tractable species where mechanisms can be more readily dissected. We evaluated the temporal- and cell-specific induction of the proneurotrophins and their receptors, including p75(NTR), sortilin, and sorCS2, following mild SE induced with kainic acid (KA) or severe SE induced by pilocarpine. We found that mature NGF, p75(NTR), and proBDNF were upregulated following SE, while proNGF was not altered, indicating potential mechanistic differences between rats and mice. ProBDNF was localized to mossy fibers and microglia following SE. p75(NTR) was transiently induced primarily in axons and axon terminals following SE, as well as in neuron and astrocyte cell bodies. ProBDNF and p75(NTR) increased independently of cell death and their localization was different depending on the severity of SE. We also examined the expression of proneurotrophin co-receptors, sortilin and sorCS2. Following severe SE, sorCS2, but not sortilin, was elevated in neurons and astrocytes. These data indicate that important differences exist between rat and mouse in the proneurotrophin response following SE. Moreover, the proBDNF and p75(NTR) increase after seizures in the absence of significant cell death suggests that proneurotrophin signaling may play other roles following SE.
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