Mitosis in Mammalion Cells during Exposure to Anesthetics

Sturrock, J.E.; Nunn, J. F.

doi:10.1097/00000542-197507000-00004

Cited by 53 publications

(12 citation statements)

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“…Finally, changes in spine morphology have been associated with alterations in the extent of the contact zone at the synaptic junction (37)(38)(39)(40). As a target for volatile anesthetics, the actin cytoskeleton may also explain some of their undesirable side effects (41,42), several of which involve actin-based mechanisms including cardiac muscle contractility (43), lymphocyte motility (44), and cell division (45).…”

Section: Discussionmentioning

confidence: 99%

Volatile anesthetics block actin-based motility in dendritic spines

Kaech

Brinkhaus

Matus

1999

Proc. Natl. Acad. Sci. U.S.A.

102

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Dendritic spines form the postsynaptic contact sites for most excitatory synapses in the brain. Spines occur in a wide range of different shapes that can vary depending on an animal's experience or behavioral status. Recently we showed that spines on living neurons can change shape within seconds in a process that depends on actin polymerization. We have now found that this morphological plasticity is blocked by inhalational anesthetics at concentrations at which they are clinically effective. These volatile compounds also block actin-based motility in fibroblasts, indicating that their action is independent of neuron-specific components and thus identifying the actin cytoskeleton as a general cellular target of anesthetic action. These observations imply that inhibition of actin dynamics at brain synapses occurs during general anesthesia and that inhalational anesthetics are capable of inf luencing the morphological plasticity of excitatory synapses in the brain.

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Section: Discussionmentioning

confidence: 99%

Volatile anesthetics block actin-based motility in dendritic spines

Kaech

Brinkhaus

Matus

1999

Proc. Natl. Acad. Sci. U.S.A.

102

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“…Moreover, many major teratogens, such as valproate and retinoic acid, exert potent antiproliferative actions in the G1 phase of the cell cycle [9]. As the antiproliferative actions of halothane have been attributed in part to a prolongation of the G1 phase [22,23], it is reasonable a Cells were exposed for a 48 h period to IC 50 drug concentrations for iso¯urane and en¯urane and 2 mM for sevo¯urane. Values are expressed as percentage of cells in each phase and are the mean 2 SEM (n = 3).…”

Section: Discussionmentioning

confidence: 99%

Antiproliferative actions of inhalational anesthetics: comparisons to the valproate teratogen

O’Leary

Bacon

Odumeru

et al. 2000

Intl J of Devlp Neuroscience

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The antiproliferative potential of the volatile anesthetics isoflurane, enflurane and sevoflurane was determined and compared to the valproate teratogen. The in vitro system employed, a G1 phase proliferative arrest endpoint in C6 glioma, has served previously to discriminate agents with known teratogenic potential in vivo. Based on estimated IC(50) values that were within twice the estimated minimum aveolar concentration value, the rank antiproliferative potency of the inhalational anesthetics employed was isoflurane=enflurane>>sevoflurane. Flow cytometric analysis of growth-arrested cell populations failed to reveal specific accumulation in any cell cycle phase and the lack of a G1 phase-specific effect was confirmed by the absence of a transient, time-dependent sialylation event in synchronized cells. The antiproliferative mechanism of volatile anesthetics, and valproate, was mediated at hydrophobic binding sites, as increasing the hydration sphere of the drug-micelle complex, using the hygroscopic qualities of the dimethylsulfoxide vehicle, completely reversed this effect. Our findings suggest inhalational anesthetics lack the specific in vitro characteristics of the valproate teratogen.

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“…At the cellular level, anaesthetics inhibit the mitotic spindle and produce c-metaphases (Sturrock andNunn 1975, 1976), and non-disjunction in Drosophila (Clements and Todd 1981). Halothane showed weak mutagenic activity in long term treatments of Drosophila, showing a slight increase in mutation frequency (Kramers andBurm 1979, Kundomal andBaden 1985).…”

Section: Discussionmentioning

confidence: 99%