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A Cambridge Neuroscience Workshop,. Department of Genetics, University of Cambridge, 20 th April ,. Talks from 2pm to 5. The aim of this workshop was to promote interactions, and better awareness of local activity, in the area of axon cell biology, across a spectrum of systems, problems and centres in Cambridge.

Potential speakers were initially nominated by the three organisers, but had the option of nominating an alternative from their group, and were invited to nominate possible additional speakers from other groups. Topics covered included membrane traffic, signalling, cytoskeleton, axon transport, axon translation, and degeneration. Attendance was high — the Genetics Part II Room has 60 seats when completely full, and virtually every seat was taken. Most participants stayed for the poster session, which was very lively — I overheard a number of participants from different groups exchanging contact details to set up further interaction.

Organisational support was provided by Dervila Glynn , and in-house by Ms. Roz McKenzie from the Genetics Department — who worked together seamlessly and effectively to ensure that the event came off smoothly, despite an over-running Genetics Building refurbishment. Thanks are due to them, and also to Mr.

Cell Biology of the axon: progress made and promises ahead

The ability to culture CNS neurons RGC that produce abundant axon growth in compartmented culture dishes is an important advance and offers several advantages over presently available systems for culturing CNS neurons. First, RGC are primary, post-mitotic neurons, and the cultures are essentially devoid of other cell types These neurons extend long axons, a characteristic that facilitates their growth in compartmented dishes.

The two side compartments contain pure distal axons, without cell bodies and dendrites Fig. Distal axons can be removed and the rate of axon regeneration can be accurately measured. Another important feature is that cell bodies and distal axons can be exposed to different milieu so that metabolic events occurring in distal axons can be modulated independently of those in cell bodies. Pure distal axons can also be harvested for biochemical measurements such as immunoblotting, enzymatic assays, and radiolabeling.

In addition, the compartmented culture system provides an excellent opportunity for studying mechanisms of transport of molecules between cell bodies and distal axons 40 , This novel compartment model for culture of CNS neurons will be widely applicable to studies on the regulation of axon growth and regeneration of CNS neurons, and on the anterograde and retrograde transport of molecules between cell bodies and axons.

Glial Cell-derived Lipoproteins Stimulate Axon Growth of Retinal Ganglion Cells— Essentially all cholesterol in the brain is synthesized endogenously rather than being imported from the circulation An abundant supply of cholesterol to neurons is important for a normal rate of axon growth. Previous studies have shown that when cholesterol synthesis was inhibited in cell bodies of sympathetic neurons from rats 43 , 46 and mice 40 the rate of axon extension was decreased.

However, a normal rate of axon growth was restored when cholesterol or human low density and high density lipoproteins were provided to distal axons It is not clear, however, what proportion of the cholesterol required for neuronal functions such as axon growth is derived from endogenous synthesis in neurons and what proportion is imported from surrounding glial cells. Although phospholipids can be synthesized in distal axons, cholesterol synthesis appears to be restricted to cell bodies 38 , Consequently, cholesterol must be either anterogradely transported long distances from cell bodies to distal axons or, alternatively, imported from glial cells positioned in close proximity to the distal axons.

Enigmatically, in response to a nerve injury, cholesterol synthesis in neurons is inhibited At the same time, however, apoE synthesis in glial cells is dramatically increased 62 , This increase in apoE production by glial cells has been proposed to represent a mechanism whereby lipid transport from glial cells to neurons is increased so that cholesterol is available for repairing the injured neurons 19 , 45 , Pfrieger 65 has suggested that cholesterol synthesis in CNS neurons is down-regulated after birth, implying that under this condition most neuronal cholesterol would have to be imported from glial cells.

Based on the known ligand specificity and function of the LDLr it is generally assumed that other members of this family of receptors can also bind and internalize apoE-containing lipoproteins via endocytosis. Consequently, cholesterol associated with LP-E derived from glial cells could be endocytosed by axons and used for membrane production during axon growth. Our observations are consistent with the idea that cholesterol delivered to distal axons by glial cell-derived apoE is an important source of cholesterol for normal axon growth of CNS neurons in vivo.

There are, however, other possible mechanisms by which glial cell-derived LP-E might stimulate axon growth since some receptors of the LDLr superfamily also act as signaling receptors upon binding to their ligands, such as apoE 53 , 68 — Thus, important signaling pathways are activated in neurons by apoE-containing lipoproteins in the absence of internalization of the lipoprotein ligand.

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Importantly, in this mode of action, the receptor does not deliver lipids to the neurons. Some evidence that apoE can influence axon growth without delivering lipids came from experiments in which lipid-poor lipoproteins containing apoE3 or apoE4, but essentially no cholesterol, elicited differential effects on neurite growth of Neuro2a cells 31 , In the present study, apoE alone, devoid of associated lipid, failed to stimulate axon extension of RGC. However, we are unable to conclude from this observation that cholesterol delivery from LP-E is required for stimulation of axon growth because lipid-free apoE appears not to be in the correct conformation for binding efficiently to the LDLr 24 or probably to other members of this receptor family.

Consequently, our studies do not distinguish whether the growth stimulatory effect of glial LP-E is the result of lipid delivery to the axon or is due to activation of a signaling pathway that stimulates axon growth. However, since RAP abrogates the growth stimulatory effect of glia-derived lipoproteins on RGC, we conclude that apoE-containing lipoproteins stimulate growth by binding to receptors of the LDLr family. An exciting possibility is that the compartmented culture technique will, in the future, be applicable to CNS neurons e. RGC derived from genetically modified mice e.

Studies using these neurons would likely provide further mechanistic insight into the role of glial cell-derived lipoproteins in axon extension. 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 — 7 , In support of this concept, a recent study showed that cholesterol- and sphingolipid-rich lipid rafts are abundant in dendrites of cultured hippocampal neurons and that depletion of cholesterol and rafts leads to gradual loss of synapses and dendritic spines The present study demonstrates for the first time that apoE-containing lipoproteins secreted from glial cells stimulate axon growth of CNS neurons when applied locally to distal axons.

The costs of publication of this article were defrayed in part by the payment of page charges. Section solely to indicate this fact.

Glia to axon RNA transfer

You'll be in good company. Journal of Lipid Research. Previous Section Next Section. Previous Section. Campenot, R. Vernadakis, A. CrossRef Medline Google Scholar. Barres, B. Pfrieger, F.

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