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1.
Neuroscience ; 284: 555-565, 2015 Jan 22.
Artículo en Inglés | MEDLINE | ID: mdl-25450957

RESUMEN

Motor deficits are present in cardiac arrest survivors and injury to cerebellar Purkinje cells (PCs) likely contribute to impairments in motor coordination and post-hypoxic myoclonus. N-Methyl-D-aspartic acid (NMDA) receptor-mediated excitotoxicity is a well-established mechanism of cell death in several brain regions, but the role of NMDA receptors in PC injury remains understudied. Emerging data in cortical and hippocampal neurons indicate that the GluN2A-containing NMDA receptors signal to improve cell survival and GluN2B-containing receptors contribute to neuronal injury. This study compared neuronal injury in the hippocampal CA1 region to that in PCs and investigated the role of NMDA receptors in PC injury in our mouse model of cardiac arrest and cardiopulmonary resuscitation (CA/CPR). Analysis of cell density demonstrated a 24% loss of PCs within 24 h after 8 min CA/CPR and injury stabilized to 33% by 7 days. The subunit promiscuous NMDA receptor antagonist MK-801 protected both CA1 neurons and PCs from ischemic injury following CA/CPR, demonstrating a role for NMDA receptor activation in injury to both brain regions. In contrast, the GluN2B antagonist, Co 101244, had no effect on PC loss while protecting against injury in the CA1 region. These data indicate that ischemic injury to cerebellar PCs progresses via different cell death mechanisms compared to hippocampal CA1 neurons.


Asunto(s)
Isquemia Encefálica/fisiopatología , Región CA1 Hipocampal/fisiopatología , Neuronas/fisiología , Células de Purkinje/fisiología , Receptores de N-Metil-D-Aspartato/metabolismo , Animales , Isquemia Encefálica/patología , Región CA1 Hipocampal/efectos de los fármacos , Región CA1 Hipocampal/patología , Calbindinas/metabolismo , Reanimación Cardiopulmonar , Muerte Celular/efectos de los fármacos , Muerte Celular/fisiología , Modelos Animales de Enfermedad , Maleato de Dizocilpina/farmacología , Antagonistas de Aminoácidos Excitadores/farmacología , Paro Cardíaco , Masculino , Ratones Endogámicos C57BL , Proteínas del Tejido Nervioso/antagonistas & inhibidores , Proteínas del Tejido Nervioso/metabolismo , Neuronas/efectos de los fármacos , Neuronas/patología , Fármacos Neuroprotectores/farmacología , Piperidinas/farmacología , Células de Purkinje/efectos de los fármacos , Células de Purkinje/patología , Receptores de N-Metil-D-Aspartato/antagonistas & inhibidores , Técnicas de Cultivo de Tejidos
2.
J Neurosci Methods ; 222: 34-41, 2014 Jan 30.
Artículo en Inglés | MEDLINE | ID: mdl-24192226

RESUMEN

BACKGROUND: Pediatric sudden cardiac arrest (CA) is an unfortunate and devastating condition, often leading to poor neurologic outcomes. However, little experimental data on the pathophysiology of pediatric CA is currently available due to the scarcity of animal models. NEW METHOD: We developed a novel experimental model of pediatric cardiac arrest and cardiopulmonary resuscitation (CA/CPR) using postnatal day 20-25 mice. Adult (8-12 weeks) and pediatric (P20-25) mice were subjected to 6min CA/CPR. Hippocampal CA1 and striatal neuronal injury were quantified 3 days after resuscitation by hematoxylin and eosin (H&E) and Fluoro-Jade B staining, respectively. RESULTS: Pediatric mice exhibited less neuronal injury in both CA1 hippocampal and striatal neurons compared to adult mice. Increasing ischemia time to 8 min CA/CPR resulted in an increase in hippocampal injury in pediatric mice, resulting in similar damage in adult and pediatric brains. In contrast, striatal injury in the pediatric brain following 6 or 8 min CA/CPR remained extremely low. As observed in adult mice, cardiac arrest causes delayed neuronal death in pediatric mice, with hippocampal CA1 neuronal damage maturing at 72 h after insult. Finally, mild therapeutic hypothermia reduced hippocampal CA1 neuronal injury after pediatric CA/CPR. COMPARISON WITH EXISTING METHOD: This is the first report of a cardiac arrest and CPR model of global cerebral ischemia in mice. CONCLUSIONS: Therefore, the mouse pediatric CA/CPR model we developed is unique and will provide an important new tool to the research community for the study of pediatric brain injury.


Asunto(s)
Isquemia Encefálica/etiología , Isquemia Encefálica/patología , Reanimación Cardiopulmonar , Modelos Animales de Enfermedad , Paro Cardíaco/complicaciones , Paro Cardíaco/terapia , Envejecimiento , Animales , Isquemia Encefálica/terapia , Región CA1 Hipocampal/crecimiento & desarrollo , Región CA1 Hipocampal/patología , Muerte Celular , Cuerpo Estriado/crecimiento & desarrollo , Cuerpo Estriado/patología , Eosina Amarillenta-(YS) , Fluoresceínas , Paro Cardíaco/patología , Hematoxilina , Hipotermia Inducida , Masculino , Ratones , Ratones Endogámicos C57BL , Neuronas/patología , Pediatría , Factores de Tiempo
15.
Radiologe ; 7(3): 107-8, 1967 Mar.
Artículo en Alemán | MEDLINE | ID: mdl-4871949
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