Neuronal and glial cell biology

Barres, Ben A.; Barde, Yves‐Alain

doi:10.1016/s0959-4388(00)00134-3

Cited by 100 publications

(52 citation statements)

References 67 publications

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“…Our data add to the growing body of evidence suggesting that glial cells have an intimate relationship with neurons and are important for normal neuronal functions such as neuronal excitability, synaptic transmission and synapse formation (2)(3)(4)(5)(6)(7)10). Interestingly, cholesterol in GCM promotes synapse formation in RGC, in a process most likely mediated by apoE (10).…”

Section: Receptor-associated Protein (Rap) Prevents the Gcm-mediated supporting

confidence: 61%

Glial Lipoproteins Stimulate Axon Growth of Central Nervous System Neurons in Compartmented Cultures

Hayashi

Campenot

Vance

et al. 2004

Journal of Biological Chemistry

167

132

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The role of lipoproteins secreted by cortical glial cells in axon growth of central nervous system (CNS) neurons was investigated. We first established compartmented cultures of CNS neurons (retinal ganglion cells). Addition of glial cell-conditioned medium (GCM) to distal axons increased the rate of axon extension by ϳ50%. Inhibition of 3-hydroxy-3-methylglutaryl-CoA reductase in glial cells diminished the secretion of cholesterol and apolipoprotein E, and prevented the growth stimulatory effect of GCM. When glia-derived lipoproteins containing apolipoprotein E were provided to distal axons, axon extension was stimulated to the same extent as by GCM. In contrast, addition of lipoproteins to cell bodies failed to enhance growth. The growth stimulatory effect of glial lipoproteins was abrogated in the presence of receptor-associated protein, RAP, indicating involvement of receptor(s) of the low density lipoprotein receptor family in stimulation of axonal extension. These observations suggest that glial cells stimulate axon growth of CNS neurons by providing lipoproteins containing cholesterol and apolipoprotein E to distal axons.Identification of factors that regulate axon growth and regeneration of CNS 1 neurons has been hampered by the lack of a model that recapitulates the in vivo environment. In intact animals, neuronal cell bodies and axon terminals often reside far apart in distinct environments. The issue of spatial separation of cell bodies and axons was addressed for peripheral neurons by the establishment of sympathetic neuron cultures in which cell bodies were plated in one compartment and axons extended into adjacent compartments (1). Consequently, cell bodies and distal axons could be exposed to independent fluid environments and the rate of axon extension accurately measured. Our objective was to culture CNS neurons in compartmented cultures and identify factors that stimulated axon growth.The most numerous cell types in the brain are glial cells: oligodendrocytes, astrocytes, and microglia. Glial cells interact with neurons and are associated with neuronal excitability and synaptic transmission (2) (3-7). Glial cell-conditioned medium (GCM) stimulates synapse development of CNS neurons (8, 9), and cholesterol, associated with apolipoprotein (apo) E, was identified as the factor that promotes synaptogenesis (10).ApoE is synthesized in the brain primarily by astrocytes and microglia (11-13) and is the major CNS apolipoprotein. ApoJ is also abundant in the brain (14). Cerebrospinal fluid, which is separated from the plasma compartment by the blood-brain barrier, contains a population of lipoproteins distinct from those in plasma (12,(15)(16)(17)(18). Several observations imply that apoE plays an important role in lipid metabolism in the nervous system (19). For example, apoE synthesis in glial cells dramatically increases after injury to the central (20 -22) and peripheral nervous systems (21). ApoE is also a ligand for receptors of the low density lipoprotein receptor (LDLr) superfamily, several of w...

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Section: Receptor-associated Protein (Rap) Prevents the Gcm-mediated supporting

confidence: 61%

Glial Lipoproteins Stimulate Axon Growth of Central Nervous System Neurons in Compartmented Cultures

Hayashi

Campenot

Vance

et al. 2004

Journal of Biological Chemistry

167

132

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“…The unravelling of neuroglial interactions is one of the central problems in neuroscience and neurology (Barres and Barde 2000;Gomes et al 2001;Kettenmann and Ransom 2004;Verkhratsky and Butt 2007). Glial cells perform numerous functions in the nervous system, e.g., they support and isolate neurons and organize their development.…”

Section: Introductionmentioning

confidence: 99%

Ultrastructure of neuroglial contacts in crayfish stretch receptor

Федоренко

Uzdensky

2009

Cell Tissue Res

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In order to explore neuroglial relationships in a simple nervous system, we have studied the ultrastructure of the crayfish stretch receptor, which consists of only two mechanoreceptor neurons enwrapped by glial cells. The glial envelope comprises 10-30 glial layers separated by collagen sheets. The intercellular space between the neuronal and glial membranes is generally less than 10-15 nm in width. This facilitates diffusion between neurons and glia but restricts neuron communication with the environment. Microtubule bundles passing from the dendrites to the axon through the neuron body limit vesicular transport between the perikaryon and the neuronal membrane. Numerous invaginations into the neuron cytoplasm strengthen glia binding to the neuron and shorten the diffusion pathway between them. Double-membrane vesicles containing fragments of glial, but not neuronal cytoplasm, represent the captured tips of invaginations. Specific triads, viz., "flat submembrane cisterns - vesicles - mitochondria", are presumably involved in the formation of the invaginations and double-membrane vesicles and in neuroglial exchange. The tubular lattice in the glial cytoplasm might transfer ions and metabolites between the glial layers. The integrity of the neuronal and glial membranes is impaired in some places. However, free neuroglial passage might be prevented or limited by the dense diffuse material accumulated in these regions. Thus, neuroglial exchange with cellular components might be mediated by transmembrane diffusion, especially in the invaginations and submembrane cisterns, by the formation of double-walled vesicles in which large glial masses are captured and by transfer through tubular lattices.

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“…In the brain, however, neurons are surrounded by a larger number of astrocytes, which render physical and physiological supports for neurons (23). To measure the A␤ effect under more physiological conditions, neurons were plated onto the monolayer of confluent astrocytes and processed for the same experimental treatment.…”

Section: A␤ Attenuates Glutamatergic Neurotransmission In Neuro-mentioning

confidence: 99%

β-Amyloid Enhances Glial Glutamate Uptake Activity and Attenuates Synaptic Efficacy

Ikegaya¹,

Matsuura²,

Ueno

et al. 2002

Journal of Biological Chemistry

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Although amyloid ␤-protein (A␤) has long been implicated in the pathogenesis of Alzheimer's disease, little is known about the mechanism by which A␤ causes dementia. A␤ leads to neuronal cell death in vivo and in vitro, but recent evidence suggests that the property of the amnesic characteristic of Alzheimer's disease can be explained by a malfunction of synapses rather than a loss of neurons. Here we show that prolonged treatment with A␤ augments the glutamate clearance ability of cultured astrocytes and induces a dramatic decrease in glutamatergic synaptic activity of neurons cocultured with the astrocytes. Biotinylation assay revealed that the enhancement of glutamate uptake activity was associated with an increase in cell-surface expression of GLAST, a subtype of glial glutamate transporters, without apparent changes in the total amount of GLAST. This phenomenon was blocked efficiently by actindisrupting agents. Thus, A␤-induced actin-dependent GLAST redistribution and relevant synaptic malfunction may be a cellular basis for the amnesia of Alzheimer's disease.Amyloid ␤-protein (A␤), 1 a peptide with 40 -42 residues, is a main element of senile plaque, a hallmark of Alzheimer's disease (AD) (1, 2), and is accumulated highly in the forebrain of AD patients, as well as transgenic mice overexpressing mutant ␤-amyloid precursor protein (␤APP), which develop AD-like pathology (3, 4). Although numerous studies showed that exogenously applied or endogenously produced A␤ leads to neuronal cell death, the amnesic feature of AD cannot be explained by the neuronal loss alone (5). Indeed, accumulating evidence indicates that A␤ induces severe impairment of excitatory neurotransmission in the hippocampus (6 -8) and thereby may cause memory deficits (9). In mutant ␤APP transgenic mice, such synaptic malfunction often appears in advance of A␤ plaque formation (10, 11), and cognitive deterioration is also observed without apparent neurodegeneration (4, 12). A␤-induced synaptic deterioration rather than neuronal loss is, therefore, likely to be a main cause of early AD dementia (5, 13). However, the mechanisms by which A␤ causes such synaptic malfunction remain to be elucidated.Excitatory neurotransmission is tightly regulated by a rapid clearance of the neurotransmitter glutamate from the extracellular milieu through Na ϩ -dependent L-glutamate transporters that are expressed on astrocytes, i.e. GLAST and GLT-1 (14, 15). We therefore investigated the effect of A␤ on glutamate uptake activity in cultured cortical astrocytes. Here we show for the first time that A␤ ending at 42 residues (A␤ (1-42)) induces an increase in the activity of GLAST. This work further demonstrates that A␤ (1-42) stimulates actin-dependent GLAST redistribution from subcellular compartment to the cell surface. Such up-regulation of GLAST function may attenuate glutamatergic synaptic efficacy. EXPERIMENTAL PROCEDURESMaterials-Chemically synthesized A␤ (1-40) and A␤ (1-42) were gifts from Dr. T. Shirasawa (Department of Molecular Genetics, Tokyo Metropo...

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Neuronal and glial cell biology

Cited by 100 publications

References 67 publications

Glial Lipoproteins Stimulate Axon Growth of Central Nervous System Neurons in Compartmented Cultures

Glial Lipoproteins Stimulate Axon Growth of Central Nervous System Neurons in Compartmented Cultures

Ultrastructure of neuroglial contacts in crayfish stretch receptor

β-Amyloid Enhances Glial Glutamate Uptake Activity and Attenuates Synaptic Efficacy

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