Basic proteins in neurons containing fibrillary deposits

Exss, R; Summer, George K.

doi:10.1016/0006-8993(73)90407-1

Cited by 13 publications

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“…The intrathecal administration of aluminum salts into young rabbits causes prominent accumulations of neurofilaments (NFs) (Terry and Pena, 1965;Embree et al, 1967;Wisniewski et al, 1967;Exss and Summer, 1973;Selkoe et al, 1979;Troncoso et al, 1982;Bizzi et al, 1984;Cole et al, 1985;Bizzi and Gambetti, 1986;Muma et al, 1988) as well as abnormal phosphorylation (Bizzi and Gambetti, 1986;Troncoso et al, 1986) of NFs in the perikaryon of selected neuronal populations (Wisniewski et al, 1967;Troncoso et al, 1982), associated with a marked decrease in the axonal transport of NFs (Bizzi et al, 1984;Troncoso et al, 1985). In anterior horn cells, levels of mRNAs for all three NF proteins fall markedly, with a moderate reduction in levels of tubulin mRNA, as assessed both by in situ hybridization and Northern analysis (Muma et al, 1988).…”

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Aluminum-induced neurofilamentous changes in cultured rat dorsal root ganglia explants

et al. 1992

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Intrathecal administration of aluminum (AI) salts to susceptible species causes prominent accumulations of neurofilaments (NFs) in neurons of the CNS. Involved nerve cells display abnormal phosphorylation of perikaryal NFs, impaired axonal transport of NFs, and reduced levels of mRNA for NF proteins. Further understanding of the pathogenesis of AI toxicity has been limited by difficulties inherent in the available in vivo systems. For this reason, we have developed a model to study the effects of AI on cultured sensory neurons. Explant cultures of rat dorsal root ganglia (DRG) were exposed to 1 mM aluminum lactate for 1 d, 3 d, or 7 d and then examined morphologically. Accumulations of NFs were noted as early as 1 d after exposure, and prominent masses of NFs were seen at 3 and 7 d. Northern analysis of mRNA extracted from the cultured ganglia showed that high, medium, and low molecular weight NF protein mRNA levels were markedly reduced compared to control values by 1 d of exposure. Class II beta- tubulin mRNA was also moderately decreased. Reversibility of toxicity was assessed by removing the aluminum lactate from the medium after a 3 d exposure and examining the cultures 1 week later. The perikaryal masses of NFs dispersed and the levels of mRNA coding for the NF proteins and class II beta-tubulin increased. The neurotoxic effects of AI on cultured DRG recapitulates the effects of intrathecal administration of AI on animals; this model produces similar changes in neuronal morphology with neurofilamentous masses and similar modifications of NF gene expression.(ABSTRACT TRUNCATED AT 250 WORDS)

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Aluminum-induced neurofilamentous changes in cultured rat dorsal root ganglia explants

et al. 1992

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“…Miller and Levine (1974) also found increased incorporation of labeled leucine into protein and decreased RNA content of cultured neuroblastoma cells in which neurofibrillary tangles had been induced by aluminum salt. A neuron-enriched fraction isolated from aluminum-injected rabbits was found by Exss and Summer (1973) to have an increased uptake of ["]leucine.…”

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confidence: 99%

Effect of experimental colchicine encephalopathy on brain protein synthesis and tubulin metabolism

McMartin

Schedlbauer

1978

J. Neurobiol.

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Colchicine blocks axoplasmic flow and produces neurofibrillary degeneration. Brain slices from mice injected intracerebrally with colchicine incorporated more [14C]leucine into protein and had a decreased uptake of [14C]leucine into the perchloric acid-soluble pool than did their controls. Brain RNA content was decreased and free leucine increased by colchicine-induced encephalopathy. The specific activities of proteins from subcellular fractions of colchicine-injected brain were increased in the nuclear fraction, the 100,000-g supernatant, and its vinblastine-precipitable tubulin. The ratio of the specific activity of the crude mitochondrial fraction to that of the total homogenate was decreased, as would be consistent with impaired movement of newly labeled protein into synaptosomes. Colchicine-injected brain extracts contained one or more cytosol fractions that stimulated ribosomal incorporation of [14C]leucine into protein in a cell-free system. Colchicine-binding-activity measurements indicated loss of soluble and particulate tubulin in colchicine-injected brains; the decrease of soluble tubulin was verified by its selective precipitation with vinblastine. Colchicine encephalopathy did not affect the rate of spontaneous breakdown of in vitro colchicine binding activity. Similarities of colchicine encephalopathy to the neuron's response to axonal damage suggest that colchicine-induced increase in protein synthesis may, in part, reflect a neuronal response to blockage of neuroplasmic transport.

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Aluminum and the Genetic Apparatus in Alzheimer Disease

Crapper

Boni

1977

Advances in Behavioral Biology

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Basic proteins in neurons containing fibrillary deposits

Cited by 13 publications

References 30 publications

Aluminum-induced neurofilamentous changes in cultured rat dorsal root ganglia explants

Aluminum-induced neurofilamentous changes in cultured rat dorsal root ganglia explants

Effect of experimental colchicine encephalopathy on brain protein synthesis and tubulin metabolism

Aluminum and the Genetic Apparatus in Alzheimer Disease

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