دورية أكاديمية
Preventing Long-Term Brain Damage by Nerve Agent-Induced Status Epilepticus in Rat Models Applicable to Infants: Significant Neuroprotection by Tezampanel Combined with Caramiphen but Not by Midazolam Treatment.
| العنوان: | Preventing Long-Term Brain Damage by Nerve Agent-Induced Status Epilepticus in Rat Models Applicable to Infants: Significant Neuroprotection by Tezampanel Combined with Caramiphen but Not by Midazolam Treatment. |
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| المؤلفون: | De Araujo Furtado M; Departments of Anatomy, Physiology, and Genetics (M.D.A.F., V.A.-A., T.H.F., V.I.P., K.R., M.F.M.B.) and Psychiatry (V.A.-A., M.F.M.B.), F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland; and Neuroscience Branch, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, Gunpowder, Maryland (J.P.A.)., Aroniadou-Anderjaska V; Departments of Anatomy, Physiology, and Genetics (M.D.A.F., V.A.-A., T.H.F., V.I.P., K.R., M.F.M.B.) and Psychiatry (V.A.-A., M.F.M.B.), F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland; and Neuroscience Branch, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, Gunpowder, Maryland (J.P.A.)., Figueiredo TH; Departments of Anatomy, Physiology, and Genetics (M.D.A.F., V.A.-A., T.H.F., V.I.P., K.R., M.F.M.B.) and Psychiatry (V.A.-A., M.F.M.B.), F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland; and Neuroscience Branch, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, Gunpowder, Maryland (J.P.A.)., Pidoplichko VI; Departments of Anatomy, Physiology, and Genetics (M.D.A.F., V.A.-A., T.H.F., V.I.P., K.R., M.F.M.B.) and Psychiatry (V.A.-A., M.F.M.B.), F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland; and Neuroscience Branch, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, Gunpowder, Maryland (J.P.A.)., Apland JP; Departments of Anatomy, Physiology, and Genetics (M.D.A.F., V.A.-A., T.H.F., V.I.P., K.R., M.F.M.B.) and Psychiatry (V.A.-A., M.F.M.B.), F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland; and Neuroscience Branch, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, Gunpowder, Maryland (J.P.A.)., Rossetti K; Departments of Anatomy, Physiology, and Genetics (M.D.A.F., V.A.-A., T.H.F., V.I.P., K.R., M.F.M.B.) and Psychiatry (V.A.-A., M.F.M.B.), F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland; and Neuroscience Branch, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, Gunpowder, Maryland (J.P.A.)., Braga MFM; Departments of Anatomy, Physiology, and Genetics (M.D.A.F., V.A.-A., T.H.F., V.I.P., K.R., M.F.M.B.) and Psychiatry (V.A.-A., M.F.M.B.), F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland; and Neuroscience Branch, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, Gunpowder, Maryland (J.P.A.) maria.braga@usuhs.edu. |
| المصدر: | The Journal of pharmacology and experimental therapeutics [J Pharmacol Exp Ther] 2024 Jan 17; Vol. 388 (2), pp. 432-450. Date of Electronic Publication: 2024 Jan 17. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural |
| اللغة: | English |
| بيانات الدورية: | Publisher: American Society for Pharmacology and Experimental Therapeutics Country of Publication: United States NLM ID: 0376362 Publication Model: Electronic Cited Medium: Internet ISSN: 1521-0103 (Electronic) Linking ISSN: 00223565 NLM ISO Abbreviation: J Pharmacol Exp Ther Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: 1999- : Bethesda, MD : American Society for Pharmacology and Experimental Therapeutics Original Publication: Baltimore : Williams & Wilkins |
| مواضيع طبية MeSH: | Nerve Agents*/toxicity , Soman*/toxicity , Status Epilepticus*/chemically induced , Status Epilepticus*/drug therapy , Brain Injuries*/chemically induced , Brain Injuries*/drug therapy , Neuroprotective Agents*/pharmacology , Neuroprotective Agents*/therapeutic use , Cyclopentanes* , Isoquinolines* , Tetrazoles*, Humans ; Infant, Newborn ; Rats ; Animals ; Midazolam/pharmacology ; Midazolam/therapeutic use ; Neuroprotection ; Rats, Sprague-Dawley ; Seizures/drug therapy ; Anticonvulsants/adverse effects ; Brain ; Atrophy/drug therapy |
| مستخلص: | Acute exposure to nerve agents induces a peripheral cholinergic crisis and prolonged status epilepticus (SE), causing death or long-term brain damage. To provide preclinical data pertinent to the protection of infants and newborns, we compared the antiseizure and neuroprotective effects of treating soman-induced SE with midazolam (MDZ) versus tezampanel (LY293558) in combination with caramiphen (CRM) in 12- and 7-day-old rats. The anticonvulsants were administered 1 hour after soman exposure; neuropathology data were collected up to 6 months postexposure. In both ages, the total duration of SE within 24 hours after soman exposure was significantly shorter in the LY293558 plus CRM groups compared with the MDZ groups. Neuronal degeneration was substantial in the MDZ-treated groups but absent or minimal in the groups treated with LY293558 plus CRM. Loss of neurons and interneurons in the basolateral amygdala and CA1 hippocampal area was significant in the MDZ-treated groups but virtually absent in the LY293558 plus CRM groups. Atrophy of the amygdala and hippocampus occurred only in MDZ-treated groups. Neuronal/interneuronal loss and atrophy of the amygdala and hippocampus deteriorated over time. Reduction of inhibitory activity in the basolateral amygdala and increased anxiety were found only in MDZ groups. Spontaneous recurrent seizures developed in the MDZ groups, deteriorating over time; a small percentage of rats from the LY293558 plus CRM groups also developed seizures. These results suggest that brain damage can be long lasting or permanent if nerve agent-induced SE in infant victims is treated with midazolam at a delayed timepoint after SE onset, whereas antiglutamatergic treatment with tezampanel and caramiphen provides significant neuroprotection. SIGNIFICANCE STATEMENT: To protect the brain and the lives of infants in a mass exposure to nerve agents, an anticonvulsant treatment must be administered that will effectively stop seizures and prevent neuropathology, even if offered with a relative delay after seizure onset. The present study shows that midazolam, which was recently approved by the Food and Drug Administration for the treatment of nerve agent-induced status epilepticus, is not an effective neuroprotectant, whereas brain damage can be prevented by targeting glutamate receptors. (U.S. Government work not protected by U.S. copyright.) |
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| معلومات مُعتمدة: | U01 NS102135 United States NS NINDS NIH HHS; U01 NS123252 United States NS NINDS NIH HHS |
| المشرفين على المادة: | 0 (Nerve Agents) 6XN50U405Y (tezampanel) R60L0SM5BC (Midazolam) 96-64-0 (Soman) 97J7NP0XJY (caramiphen) 0 (Anticonvulsants) 0 (Neuroprotective Agents) 0 (Cyclopentanes) 0 (Isoquinolines) 0 (Tetrazoles) |
| تواريخ الأحداث: | Date Created: 20230922 Date Completed: 20240119 Latest Revision: 20240313 |
| رمز التحديث: | 20240313 |
| مُعرف محوري في PubMed: | PMC10801760 |
| DOI: | 10.1124/jpet.123.001710 |
| PMID: | 37739807 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1521-0103 |
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| DOI: | 10.1124/jpet.123.001710 |