Axonal synthesis of phosphatidylcholine is required for normal axonal growth in rat sympathetic neurons.

Chaves, E; Vance, Dennis E.; Campenot, Robert B.; Vance, Jean E.

doi:10.1083/jcb.128.5.913

Cited by 74 publications

(38 citation statements)

References 28 publications

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“…For example, in cultured cells choline deficiency causes apoptosis [Albright et al, 1996;Holmes-McNary et al, 1997] and inhibits axonal growth [Posse de Chaves et al, 1995], and treatments identical to those used in the current study alter hippocampal apoptotic patterns in vivo [Holmes-McNary et al, 1997]. Prenatal choline supplementation causes a 40% elevation in fetal brain phosphocholine [Garner et al, 1995], a metabolite that serves as a storage pool of choline and which may be necessary for cell division initiated by certain growth factors [Cuadrado et al, 1993;Jiménez et al, 1995;Kiss and Mukherjee, 1997].…”

Section: Discussionmentioning

confidence: 99%

Prenatal Availability of Choline Alters the Development of Acetylcholinesterase in the Rat Hippocampus

Cermák¹,

Blusztajn²,

Meck

et al. 1999

Dev Neurosci

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Choline (Ch) supplementation during embryonic days (ED) 12–17 enhances spatial and temporal memory in adult and aged rats, whereas prenatal Ch deficiency impairs attention performance and accelerates age-related declines in temporal processing. To characterize the neurochemical and neuroanatomical mechanisms that may mediate these behavioral effects in rats, we studied the development [postnatal days (PD) 1, 3, 7, 17, 27, 35, 90, and 26 months postnatally] of acetylcholinesterase (AChE) activity in hippocampus, neocortex and striatum as a function of prenatal Ch availability. We further measured the density of AChE-positive laminae (PD27 and PD90) and interneurons (PD20) in the hippocampus as a function of prenatal Ch availability. During ED11-ED17 pregnant Sprague-Dawley rats received a Ch-deficient, control or Ch-supplemented diet (average Ch intake 0, 1.3 and 4.6 mmol/kg/day, respectively). Prenatal Ch deficiency increased hippocampal AChE activity as compared to control animals in both males and females from the 2nd to 5th week postnatally. Moreover, prenatal Ch supplementation reduced hippocampal AChE activity as compared to control animals over the same developmental period. There was no effect of prenatal Ch status on either cortical or striatal AChE activity at any age measured, and by PD90 the effect of Ch on hippocampal AChE was no longer observed. In order to localize the early changes in hippocampal AChE activity anatomically, frozen coronal brain sections (PD20, PD27, PD90) were stained histochemically for AChE. Consistent with biochemical results, the AChE staining intensity was reduced in PD27 hippocampal laminae in the Ch-supplemented group and increased in the Ch-deficient group compared to control animals. There was no effect of the diet on hippocampal AChE staining intensity on PD90. In addition, the prenatal Ch availability was found to alter the size and density of AChE-positive PD20 interneurons. These results show that prenatal Ch availability has long-term consequences on the development of the hippocampal cholinergic system.

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Section: Discussionmentioning

confidence: 99%

Prenatal Availability of Choline Alters the Development of Acetylcholinesterase in the Rat Hippocampus

Cermák¹,

Blusztajn²,

Meck

et al. 1999

Dev Neurosci

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“…Indeed, experiments carried out with in vitro preparations of growth cones have identified the existence of a population of large plasmalemma precursor vesicles that might be responsible for membrane expansion (Pfenninger and Friedman,1993). The possibility that at least the phospholipid components of the axonal plasma membrane are locally synthesized has also been raised (Posse de Chaves et al, 1995).…”

Section: Introductionmentioning

confidence: 99%

Neurite Extension Occurs in the Absence of Regulated Exocytosis in PC12 Subclones

Leoni

Menegon

Benfenati

et al. 1999

MBoC

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We have investigated the process leading to differentiation of PC12 cells. This process is known to include extension of neurites and changes in the expression of subsets of proteins involved in cytoskeletal rearrangements or in neurosecretion. To this aim, we have studied a PC12 clone (trk-PC12) stably transfected with the nerve growth factor receptor TrkA. These cells are able to undergo both spontaneous and neurotrophin-induced morphological differentiation. However, both undifferentiated and nerve growth factor-differentiated trk-PC12 cells appear to be completely defective in the expression of proteins of the secretory apparatus, including proteins of synaptic vesicles and large dense-core granules, neurotransmitter transporters, and neurotransmitter-synthesizing enzymes. These results indicate that neurite extension can occur independently of the presence of the neurosecretory machinery, including the proteins that constitute the fusion machine, suggesting the existence of differential activation pathways for the two processes during neuronal differentiation. These findings have been confirmed in independent clones obtained from PC12-27, a previously characterized PC12 variant clone globally incompetent for regulated secretion. In contrast, the integrity of the Rab cycle appears to be necessary for neurite extension, because antisense oligonucleotides against the neurospecific isoform of Rab-guanosine diphosphate-dissociation inhibitor significantly interfere with process formation.

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“…10); we also recently have shown that ongoing GlcCer synthesis is required for basic fibroblast growth factor and laminin to stimulate axonal growth in hippocampal neurons (Boldin and Futerman, 1997). Similarly, phosphatidylcholine (PC) synthesis is required for the growth of sympathetic neurons (de Chaves et al, 1995). PC comprises ϳ40 -50% of total neuronal membrane lipids (Siegel et al, 1994), whereas SLs comprise between 15-20%.…”

Section: A Role For Glccer In Axon Growthmentioning

confidence: 99%

Distinct Roles for Ceramide and Glucosylceramide at Different Stages of Neuronal Growth

1997

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Sphingolipids (SLs) are important structural and regulatory components of neuronal plasma membranes. Previous studies using fumonisin B 1 , an inhibitor of the synthesis of ceramide, the precursor of all SLs, demonstrated that ceramide synthesis is required to sustain axonal growth in hippocampal neurons (Harel and Futerman, 1993;Schwarz et al., 1995) and dendritic growth in cerebellar Purkinje cells (Furuya et al., 1995). We now show that ceramide plays distinct roles at different stages of neuronal development. (1) During axon growth, ceramide must be metabolized to glucosylceramide (GlcCer) to sustain growth. Thus, whereas D-erythro-ceramide, which is metabolized to GlcCer, is able to antagonize the disruptive effects of fumonisin B 1 on axon growth, L-threo-ceramide, which is not metabolized to GlcCer, is ineffective. (2) The formation of minor processes from lamellipodia can be stimulated by incubation with shortacyl chain analogs of ceramide that are active in ceramidemediated signaling pathways, or by generation of endogenous ceramide by incubation with sphingomyelinase. However, GlcCer synthesis is not required for this initial stage of neuronal development. (3) During minor process formation and during axon growth, incubation with high concentrations of ceramide or sphingomyelinase, but not dihydroceramide, induces apoptosis. Together, these observations are consistent with the possibility that minor process formation and apoptosis can be regulated by ceramide-dependent signaling pathways and that the decision whether to enter these diametrically opposed pathways depends on intracellular ceramide concentrations. In contrast, axonal growth requires the synthesis of GlcCer from ceramide, perhaps to support an intracellular transport pathway.

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Axonal synthesis of phosphatidylcholine is required for normal axonal growth in rat sympathetic neurons.

Cited by 74 publications

References 28 publications

Prenatal Availability of Choline Alters the Development of Acetylcholinesterase in the Rat Hippocampus

Prenatal Availability of Choline Alters the Development of Acetylcholinesterase in the Rat Hippocampus

Neurite Extension Occurs in the Absence of Regulated Exocytosis in PC12 Subclones

Distinct Roles for Ceramide and Glucosylceramide at Different Stages of Neuronal Growth

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