{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,31]],"date-time":"2026-10-31T04:41:05Z","timestamp":1793421665464,"version":"4.5.0"},"reference-count":40,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2014,5,7]],"date-time":"2014-05-07T00:00:00Z","timestamp":1399420800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["R01NS051710"],"award-info":[{"award-number":["R01NS051710"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100002736","name":"Citizens United for Research in Epilepsy","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100002736","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100001605","name":"Epilepsy Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100001605","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100001454","name":"American Epilepsy Society","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100001454","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2014,10]]},"abstract":"<jats:p>\n                    Neurotrophins, such as brain\u2010derived neurotrophic factor (BDNF), are initially expressed in a precursor form (e.g., pro\u2010BDNF) and cleaved to form mature BDNF (mBDNF). After pilocarpine\u2010induced status epilepticus (SE), increases in neurotrophins regulate a wide variety of cell\u2010signaling pathways, including prosurvival and cell\u2010death machinery in a receptor\u2010specific manner. Pro\u2010BDNF preferentially binds to the p75 neurotrophin receptor (p75\n                    <jats:sup>NTR<\/jats:sup>\n                    ), whereas mBDNF is the major ligand of the tropomyosin\u2010related kinase receptor. To elucidate a potential role for p75\n                    <jats:sup>NTR<\/jats:sup>\n                    in acute stages of epileptogenesis, rats were injected prior to and at onset of SE with LM11A\u201031, a small\u2010molecule ligand that binds to p75\n                    <jats:sup>NTR<\/jats:sup>\n                    to promote survival signaling and inhibit neuronal cell death. Modulation of early p75\n                    <jats:sup>NTR<\/jats:sup>\n                    signaling and its effects on electrographic SE, SE\u2010induced neurodegeneration, and subsequent spontaneous seizures were examined after LM11A\u201031 administration. Despite an established neuroprotective effect of LM11A\u201031 in several animal models of neurodegenerative disorders (e.g., Alzheimer's disease, traumatic brain injury, and spinal cord injury), high\u2010dose LM11A\u201031 administration prior to and at onset of SE did not reduce the intensity of electrographic SE, prevent SE\u2010induced neuronal cell injury, or inhibit the progression of epileptogenesis. Further studies are required to understand the role of p75\n                    <jats:sup>NTR<\/jats:sup>\n                    activation during epileptogenesis and in seizure\u2010induced cell injury in the hippocampus, among other potential cellular pathologies contributing to the onset of spontaneous seizures. Additional studies utilizing more prolonged treatment with LM11A\u201031 are required to reach a definite conclusion on its potential neuroprotective role in epilepsy. \u00a9 2014 Wiley Periodicals, Inc.\n                  <\/jats:p>","DOI":"10.1002\/jnr.23402","type":"journal-article","created":{"date-parts":[[2014,5,7]],"date-time":"2014-05-07T04:23:51Z","timestamp":1399436631000},"page":"1307-1318","source":"Crossref","is-referenced-by-count":18,"title":["Acute administration of the small\u2010molecule p75\n                    <sup>NTR<\/sup>\n                    ligand does not prevent hippocampal neuron loss or development of spontaneous seizures after pilocarpine\u2010induced status epilepticus"],"prefix":"10.1002","volume":"92","author":[{"given":"H.L.","family":"Grabenstatter","sequence":"first","affiliation":[{"name":"Department of Pediatrics Division of Neurology and Translational Epilepsy Research Program University of Colorado School of Medicine Aurora 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