Effects of Elevated Plasma Magnesium Concentration on Cerebrospinal Fluid Levels of Magnesium in Neonatal Swine

Rivera, L I; Gootman, Phyllis M.; Lin, Roy-Hoh; Gootman, Norman

doi:10.3181/00379727-197-43231

Cited by 7 publications

(2 citation statements)

References 11 publications

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“…Neuroprotection was also demonstrated against cerebral ischemia perinatal (11,12) rat model. Blood-brain barrier is permeable to magnesium in neonatal swine (13).…”

Section: Introductionmentioning

confidence: 99%

Effects of Magnesium Sulfate Administration During Hypoxia on Ca2+ Influx and IP3 Receptor Modification in Cerebral Cortical Neuronal Nuclei of Newborn Piglets

et al. 2006

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Magnesium is a non-competitive antagonist of the NMDA receptor. Hypoxic insults to the brain are associated with a significant increase in the intranuclear Ca(2+) due to altered nuclear membrane Ca(2+) influx mechanisms including hypoxia-induced modifications of nuclear membrane IP(3) receptors. In this study we have examined the effects of magnesium sulfate administration to newborn piglets subjected to normoxia and severe hypoxia. The animals were randomly divided into normoxic (n=4), hypoxic (n=4) and magnesium sulfate treated hypoxic (n=4) groups. Hypoxia was confirmed biochemically by measuring ATP and phosphocreatine (PCr) levels in the brain tissue. Intranuclear Ca(2+) influx was assessed by measuring (45)Ca(2+) uptake. Results show a significant (P<0.05) decrease in ATP and PCr levels in hypoxic group in comparison with normoxia. On the other hand magnesium-treated hypoxic group showed a significantly (P<0.05) higher ATP and PCr in comparison with the hypoxic group. Intranuclear Ca(2+) was significantly (P<0.05) higher in the hypoxic group in comparison with both normoxic and magnesium-treated hypoxic groups. In addition results show that magnesium prevented hypoxia-induced modification of the IP(3) receptor. Magnesium treatment significantly reduced the hypoxia-induced increase in the number of receptors (reduced B(max) --P<0.05-treated hypoxia vs. hypoxia and normoxia), and reversed the receptor affinity (reduced dissociation coefficient-K(d)--P<0.05-treated hypoxia vs. normoxia). The results demonstrate that the administration of magnesium sulfate prior to hypoxia prevents the hypoxia-induced increase in intranuclear Ca(2+) and IP(3) receptor modifications. We conclude that Mg(2+ )administration prevents hypoxia-induced modification of neuronal nuclear membrane function that leads to intranuclear Ca(2+)-dependent transcription of apoptotic proteins leading to hypoxic neuronal programmed cell death.

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“…Neuroprotection was also demonstrated against cerebral ischemia perinatal (11,12) rat model. Blood-brain barrier is permeable to magnesium in neonatal swine (13).…”

Section: Introductionmentioning

confidence: 99%

Effects of Magnesium Sulfate Administration During Hypoxia on Ca2+ Influx and IP3 Receptor Modification in Cerebral Cortical Neuronal Nuclei of Newborn Piglets

et al. 2006

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“…The exact mechanism by which MgSO 4 mediates its neuroprotective effects is not fully understood, although growing evidence indicates it is at least partially due to modulation of glutamatergic signaling. MgSO 4 permeates freely across the BBB in neonatal swine ( Rivera et al, 1991 ) and non-competitively blocks NMDA receptors, reducing calcium ion intake and preventing excitotoxic cell injury and death ( Nowak et al, 1984 ; Marret et al, 1995 ). MgSO 4 reduces both NMDA-induced and hypoxia-ischemia-induced rat brain injury and accelerates the differentiation of oligodendrocytes ( McDonald et al, 1990 ; Thordstein et al, 1993 ; Kang et al, 2011 ; Itoh et al, 2016 ).…”

Section: Magnesium Sulfatementioning

confidence: 99%

Fetal Neuroprotective Strategies: Therapeutic Agents and Their Underlying Synaptic Pathways

Elsayed

Boyer

Burd

2021

Front. Synaptic Neurosci.

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Synaptic signaling is integral for proper brain function. During fetal development, exposure to inflammation or mild hypoxic-ischemic insult may lead to synaptic changes and neurological damage that impairs future brain function. Preterm neonates are most susceptible to these deleterious outcomes. Evaluating clinically used and novel fetal neuroprotective measures is essential for expanding treatment options to mitigate the short and long-term consequences of fetal brain injury. Magnesium sulfate is a clinical fetal neuroprotective agent utilized in cases of imminent preterm birth. By blocking N-methyl-D-aspartate receptors, magnesium sulfate reduces glutamatergic signaling, which alters calcium influx, leading to a decrease in excitotoxicity. Emerging evidence suggests that melatonin and N-acetyl-L-cysteine (NAC) may also serve as novel putative fetal neuroprotective candidates. Melatonin has important anti-inflammatory and antioxidant properties and is a known mediator of synaptic plasticity and neuronal generation. While NAC acts as an antioxidant and a precursor to glutathione, it also modulates the glutamate system. Glutamate excitotoxicity and dysregulation can induce perinatal preterm brain injury through damage to maturing oligodendrocytes and neurons. The improved drug efficacy and delivery of the dendrimer-bound NAC conjugate provides an opportunity for enhanced pharmacological intervention. Here, we review recent literature on the synaptic pathways underlying these therapeutic strategies, discuss the current gaps in knowledge, and propose future directions for the field of fetal neuroprotective agents.

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Anxiolytic effect of chronic intake of supplemental magnesium chloride in rat

Macías-Carballo

Rosas-Navarro

López‐Meraz

et al. 2021

Behavioural Brain Research

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Effects of Elevated Plasma Magnesium Concentration on Cerebrospinal Fluid Levels of Magnesium in Neonatal Swine

Cited by 7 publications

References 11 publications

Effects of Magnesium Sulfate Administration During Hypoxia on Ca2+ Influx and IP3 Receptor Modification in Cerebral Cortical Neuronal Nuclei of Newborn Piglets

Effects of Magnesium Sulfate Administration During Hypoxia on Ca2+ Influx and IP3 Receptor Modification in Cerebral Cortical Neuronal Nuclei of Newborn Piglets

Fetal Neuroprotective Strategies: Therapeutic Agents and Their Underlying Synaptic Pathways

Anxiolytic effect of chronic intake of supplemental magnesium chloride in rat

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