Daher Ismaël, Le Dieu-Lugon Bérénice, Dourmap Nathalie, Lecuyer Matthieu, Ramet Lauriane, Gomila Cathy, Ausseil Jérôme, Marret Stéphane, Leroux Philippe, Roy Vincent, El Mestikawy Salah, Daumas Stéphanie, Gonzalez Bruno, Leroux-Nicollet Isabelle, Cleren Carine
Department of Neonatal Pediatrics and Intensive Care - Neuropediatrics, Normandie Univ, UNIROUEN, INSERM U1245, and Rouen University Hospital, Rouen, France; Normal and Pathological Glutamatergic Systems, Neuroscience Paris Seine, IBPS, INSERM U1130, CNRS UMR 8246 Université Pierre et Marie Curie, Paris, France; INSERM U1088, Laboratoire de Biochimie, Centre de Biologie Humaine, Amiens-Picardie University Hospital, Amiens, France; Normandie Univ, UNIROUEN, PSY-NCA, Rouen, France.
J Neuropathol Exp Neurol. 2017 Oct 1;76(10):883-897. doi: 10.1093/jnen/nlx073.
Magnesium sulfate (MgSO4) administration to mothers at risk of preterm delivery is proposed as a neuroprotective strategy against neurological alterations such as cerebral palsy in newborns. However, long-term beneficial or adverse effects of MgSO4 and sex-specific sensitivity remain to be investigated. We conducted behavioral and neurochemical studies of MgSO4 effects in males and females, from the perinatal period to adolescence in a mouse model of cerebral neonatal lesion. The lesion was produced in 5-day-old (P5) pups by ibotenate intracortical injection. MgSO4 (600 mg/kg, i.p.) prior to ibotenate prevented lesion-induced sensorimotor alterations in both sexes at P6 and P7. The lesion increased glutamate level at P10 in the prefrontal cortex, which was prevented by MgSO4 in males. In neonatally lesioned adolescent mice, males exhibited more sequelae than females in motor and cognitive functions. In the perirhinal cortex of adolescent mice, the neonatal lesion induced an increase in vesicular glutamate transporter 1 density in males only, which was negatively correlated with cognitive scores. Long-term sequelae were prevented by neonatal MgSO4 administration. MgSO4 never induced short- or long-term deleterious effect on its own. These results also strongly suggest that sex-specific neuroprotection should be foreseen in preterm infants.
向有早产风险的母亲施用硫酸镁(MgSO4)被提议作为一种神经保护策略,以对抗新生儿的神经功能改变,如脑瘫。然而,硫酸镁的长期有益或有害影响以及性别特异性敏感性仍有待研究。我们在新生儿脑损伤小鼠模型中,对从围产期到青春期的雄性和雌性小鼠进行了硫酸镁作用的行为和神经化学研究。在5日龄(P5)幼崽中通过皮层内注射鹅膏蕈氨酸产生脑损伤。在注射鹅膏蕈氨酸之前给予硫酸镁(600mg/kg,腹腔注射)可预防P6和P7时损伤诱导的两性感觉运动改变。损伤使P10时前额叶皮质中的谷氨酸水平升高,而硫酸镁可预防雄性小鼠的这种升高。在新生期脑损伤的青春期小鼠中,雄性在运动和认知功能方面比雌性表现出更多后遗症。在青春期小鼠的梨状皮质中,新生期损伤仅在雄性小鼠中诱导囊泡谷氨酸转运体1密度增加,这与认知评分呈负相关。新生儿期给予硫酸镁可预防长期后遗症。硫酸镁本身从未诱导短期或长期有害影响。这些结果还强烈表明,应预见到对早产儿的性别特异性神经保护。