Early Exposure to General Anesthesia Causes Significant Neuronal Deletion in the Developing Rat Brain
Frequent exposure of children to general anesthesia is common practice in modern medicine. Although previously unrecognized, recent in vitro and in vivo animal studies suggest that exposure to clinically relevant general anesthetics at the peak of brain development could be detrimental to immature m...
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| Published in: | Annals of the New York Academy of Sciences Vol. 1122; no. 1; pp. 69 - 82 |
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01-12-2007
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| Abstract | Frequent exposure of children to general anesthesia is common practice in modern medicine. Although previously unrecognized, recent in vitro and in vivo animal studies suggest that exposure to clinically relevant general anesthetics at the peak of brain development could be detrimental to immature mammalian neurons, as demonstrated by massive and widespread apoptotic neurodegeneration. The survival of the developing neurons presumably depends on proper and timely formation of synapses, for which synaptic proteins (e.g., synaptophysin, synaptobrevin, amphiphysin, synaptosomal‐associated protein 25 [SNAP‐25], and Ca2+/calmodulin‐dependent protein kinase II [CaM kinase II]) are crucially important. Overinhibition of developing neurons impairs synaptic protein function and activity‐induced synaptic plasticity, which could in turn result in permanent neuronal loss. To examine the effects of general anesthesia, the pharmacological agents known to cause extensive neuronal inhibition, on synaptic proteins, and neuronal survival at the peak of synaptogenesis, we exposed 7‐day‐old rat pups to general anesthesia (midazolam, 9 mg/kg of body weight, subcutaneously, followed by 6 h of nitrous oxide 75 vol% and isoflurane 0.75 vol%). We found that this general anesthesia causes permanent neuronal deletion in the most vulnerable brain regions—the cerebral cortex and the thalamus—while transiently modulating protein levels of synaptophysin, synaptobrevin, amphiphysin, SNAP‐25, and CaM kinase II. |
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| AbstractList | Frequent exposure of children to general anesthesia is common practice in modern medicine. Although previously unrecognized, recent in vitro and in vivo animal studies suggest that exposure to clinically relevant general anesthetics at the peak of brain development could be detrimental to immature mammalian neurons, as demonstrated by massive and widespread apoptotic neurodegeneration. The survival of the developing neurons presumably depends on proper and timely formation of synapses, for which synaptic proteins (e.g., synaptophysin, synaptobrevin, amphiphysin, synaptosomal-associated protein 25 [SNAP-25], and Ca super(2+)/calmodulin-dependent protein kinase II [CaM kinase II]) are crucially important. Overinhibition of developing neurons impairs synaptic protein function and activity-induced synaptic plasticity, which could in turn result in permanent neuronal loss. To examine the effects of general anesthesia, the pharmacological agents known to cause extensive neuronal inhibition, on synaptic proteins, and neuronal survival at the peak of synaptogenesis, we exposed 7-day-old rat pups to general anesthesia (midazolam, 9mg/kg of body weight, subcutaneously, followed by 6h of nitrous oxide 75 vol% and isoflurane 0.75 vol%). We found that this general anesthesia causes permanent neuronal deletion in the most vulnerable brain regions-the cerebral cortex and the thalamus-while transiently modulating protein levels of synaptophysin, synaptobrevin, amphiphysin, SNAP-25, and CaM kinase II. Frequent exposure of children to general anesthesia is common practice in modern medicine. Although previously unrecognized, recent in vitro and in vivo animal studies suggest that exposure to clinically relevant general anesthetics at the peak of brain development could be detrimental to immature mammalian neurons, as demonstrated by massive and widespread apoptotic neurodegeneration. The survival of the developing neurons presumably depends on proper and timely formation of synapses, for which synaptic proteins (e.g., synaptophysin, synaptobrevin, amphiphysin, synaptosomal‐associated protein 25 [SNAP‐25], and Ca2+/calmodulin‐dependent protein kinase II [CaM kinase II]) are crucially important. Overinhibition of developing neurons impairs synaptic protein function and activity‐induced synaptic plasticity, which could in turn result in permanent neuronal loss. To examine the effects of general anesthesia, the pharmacological agents known to cause extensive neuronal inhibition, on synaptic proteins, and neuronal survival at the peak of synaptogenesis, we exposed 7‐day‐old rat pups to general anesthesia (midazolam, 9 mg/kg of body weight, subcutaneously, followed by 6 h of nitrous oxide 75 vol% and isoflurane 0.75 vol%). We found that this general anesthesia causes permanent neuronal deletion in the most vulnerable brain regions—the cerebral cortex and the thalamus—while transiently modulating protein levels of synaptophysin, synaptobrevin, amphiphysin, SNAP‐25, and CaM kinase II. Frequent exposure of children to general anesthesia is common practice in modern medicine. Although previously unrecognized, recent in vitro and in vivo animal studies suggest that exposure to clinically relevant general anesthetics at the peak of brain development could be detrimental to immature mammalian neurons, as demonstrated by massive and widespread apoptotic neurodegeneration. The survival of the developing neurons presumably depends on proper and timely formation of synapses, for which synaptic proteins (e.g., synaptophysin, synaptobrevin, amphiphysin, synaptosomal‐associated protein 25 [SNAP‐25], and Ca 2+ /calmodulin‐dependent protein kinase II [CaM kinase II]) are crucially important. Overinhibition of developing neurons impairs synaptic protein function and activity‐induced synaptic plasticity, which could in turn result in permanent neuronal loss. To examine the effects of general anesthesia, the pharmacological agents known to cause extensive neuronal inhibition, on synaptic proteins, and neuronal survival at the peak of synaptogenesis, we exposed 7‐day‐old rat pups to general anesthesia (midazolam, 9 mg/kg of body weight, subcutaneously, followed by 6 h of nitrous oxide 75 vol% and isoflurane 0.75 vol%). We found that this general anesthesia causes permanent neuronal deletion in the most vulnerable brain regions—the cerebral cortex and the thalamus—while transiently modulating protein levels of synaptophysin, synaptobrevin, amphiphysin, SNAP‐25, and CaM kinase II. Frequent exposure of children to general anesthesia is common practice in modern medicine. Although previously unrecognized, recent in vitro and in vivo animal studies suggest that exposure to clinically relevant general anesthetics at the peak of brain development could be detrimental to immature mammalian neurons, as demonstrated by massive and widespread apoptotic neurodegeneration. The survival of the developing neurons presumably depends on proper and timely formation of synapses, for which synaptic proteins (e.g., synaptophysin, synaptobrevin, amphiphysin, synaptosomal-associated protein 25 [SNAP-25], and Ca(2+)/calmodulin-dependent protein kinase II [CaM kinase II]) are crucially important. Overinhibition of developing neurons impairs synaptic protein function and activity-induced synaptic plasticity, which could in turn result in permanent neuronal loss. To examine the effects of general anesthesia, the pharmacological agents known to cause extensive neuronal inhibition, on synaptic proteins, and neuronal survival at the peak of synaptogenesis, we exposed 7-day-old rat pups to general anesthesia (midazolam, 9 mg/kg of body weight, subcutaneously, followed by 6 h of nitrous oxide 75 vol% and isoflurane 0.75 vol%). We found that this general anesthesia causes permanent neuronal deletion in the most vulnerable brain regions-the cerebral cortex and the thalamus-while transiently modulating protein levels of synaptophysin, synaptobrevin, amphiphysin, SNAP-25, and CaM kinase II. Frequent exposure of children to general anesthesia is common practice in modern medicine. Although previously unrecognized, recent in vitro and in vivo animal studies suggest that exposure to clinically relevant general anesthetics at the peak of brain development could be detrimental to immature mammalian neurons, as demonstrated by massive and widespread apoptotic neurodegeneration. The survival of the developing neurons presumably depends on proper and timely formation of synapses, for which synaptic proteins (e.g., synaptophysin, synaptobrevin, amphiphysin, synaptosomal-associated protein 25 [SNAP-25], and Ca2+/calmodulin-dependent protein kinase II [CaM kinase II]) are crucially important. Overinhibition of developing neurons impairs synaptic protein function and activity-induced synaptic plasticity, which could in turn result in permanent neuronal loss. To examine the effects of general anesthesia, the pharmacological agents known to cause extensive neuronal inhibition, on synaptic proteins, and neuronal survival at the peak of synaptogenesis, we exposed 7-day-old rat pups to general anesthesia (midazolam, 9mg/kg of body weight, subcutaneously, followed by 6h of nitrous oxide 75 vol% and isoflurane 0.75 vol%). We found that this general anesthesia causes permanent neuronal deletion in the most vulnerable brain regions-the cerebral cortex and the thalamus-while transiently modulating protein levels of synaptophysin, synaptobrevin, amphiphysin, SNAP-25, and CaM kinase II. |
| Author | JEVTOVIC-TODOROVIC, V. YON, J-H. CARTER, L. B. NIKIZAD, H. |
| Author_xml | – sequence: 1 givenname: H. surname: NIKIZAD fullname: NIKIZAD, H. organization: Department of Anesthesiology, University of Virginia Health System, Charlottesville, Virginia, USA – sequence: 2 givenname: J-H. surname: YON fullname: YON, J-H. organization: Department of Anesthesiology, University of Virginia Health System, Charlottesville, Virginia, USA – sequence: 3 givenname: L. B. surname: CARTER fullname: CARTER, L. B. organization: Department of Anesthesiology, University of Virginia Health System, Charlottesville, Virginia, USA – sequence: 4 givenname: V. surname: JEVTOVIC-TODOROVIC fullname: JEVTOVIC-TODOROVIC, V. organization: Department of Anesthesiology, University of Virginia Health System, Charlottesville, Virginia, USA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/18077565$$D View this record in MEDLINE/PubMed |
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| Title | Early Exposure to General Anesthesia Causes Significant Neuronal Deletion in the Developing Rat Brain |
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