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Gathering at the Nodes

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Gathering at the Nodes RESEARCH HIGHLIGHTS GLIA Gathering at the nodes Saltatory conduction — the process by which that are found at the nodes of Ranvier, where action potentials propagate along myelinated they interact with Na+ channels. When the nerves — depends on the fact that voltage- authors either disrupted the localization of gated Na+ channels form clusters at the nodes gliomedin by using a soluble fusion protein of Ranvier, between sections of the myelin that contained the extracellular domain of sheath. New findings from Eshed et al. show neurofascin, or used RNA interference to that Schwann cells produce a protein called suppress the expression of gliomedin, the gliomedin, and that this is responsible for characteristic clustering of Na+ channels at the clustering of these channels. the nodes of Ranvier did not occur. The formation of the nodes of Ranvier is Aggregation of the domain of gliomedin specified by the myelinating cells, not the that binds neurofascin and NrCAM on the axons, and an important component of this surface of purified neurons also caused process in the peripheral nervous system the clustering of neurofascin, Na+ channels is the extension of microvilli by Schwann and other nodal proteins. These findings cells. These microvilli contact the axons at support a model in which gliomedin on the nodes, and it is here that the Schwann References and links Schwann cell microvilli binds to neurofascin ORIGINAL RESEARCH PAPER Eshed, Y. et al. Gliomedin cells express the newly discovered protein and NrCAM on axons, causing them to mediates Schwann cell–axon interaction and the molecular gliomedin. cluster at the nodes of Ranvier, and leading assembly of the nodes of Ranvier. Neuron 47, 215–229 Eshed et al. showed that gliomedin to the formation of complexes that contain (2005) FURTHER READING Sherman, D. L. & Brophy, P. J. + is a ligand for two axonal cell adhesion Na channels. Mechanisms of axon ensheathment and myelin growth. molecules — neurofascin and NrCAM — Rachel Jones Nature Rev. Neurosci. 6, 683–690 (2005) NEUROTRANSMITTERS vesicle release at numerous sites, including postsynaptic density and non-postsynaptic density regions, while simultaneously varying the amount of acetylcholine released into the Long-distance communication synaptic cleft. The simulated mEPSCs most closely Traditionally, we have viewed neurotransmitter Recent work in the chick ciliary ganglion has resembled previously recorded mEPSCs from release as being strictly confined to presynaptic shown that one class of nicotinic acetylcholine a ciliary ganglion in situ when the model active zones and postsynaptic densities. New receptor (nAChR) — the α7-nAChRs, which included a high proportion of neurotrans- work by Coggan, Bartol and colleagues, using are located on spines — is virtually absent mitter release that occurred away from the a combination of high-resolution electron from the postsynaptic density. Nevertheless, postsynaptic density. By contrast, simulations microscopy and computational simulations, these receptors account for numerous changes in which vesicle fusion was limited to the indicates that additional neurotransmitter in physiological measurements, which indi- postsynaptic density, or when α7-nAChRs release distant from these sites (ectopic neuro- cates that they must be involved in neurotrans- were included in the postsynaptic density, transmitter release) is necessary to activate mitter responses. Furthermore, electron elicited mEPSCs that were at odds with the certain receptors. microscopy has shown presynaptic vesicles experimental recordings. that are ready for neurotransmitter release This intriguing finding challenges previous and fusing vesicles at locations distant from assumptions about the structure and function the postsynaptic density. However, until now, of synapses. So far, the reason for ectopic neu- there has been no experimental confirmation rotransmitter release specifically in the ciliary of ectopic neurotransmitter release during ganglion is unclear, but the authors speculate synaptic transmission. that it might relate to the specialized molecular Coggan, Bartol and co-workers used and physiological properties of α7-nAChRs. It electron microscopy studies to create a geo- will be interesting to determine whether this metrically accurate three-dimensional model mechanism for neurotransmitter release is of a ciliary ganglion synapse, and, on the exclusive to the ciliary ganglion or whether it basis of previous work, incorporated into the occurs during the activation of other types of model information about the distribution receptor. and kinetic properties of presynaptic release Alison Rowan sites, acetylcholinesterase and α7-nAChRs. References and links ORIGINAL RESEARCH PAPER Coggan, J. S. & Bartol, T. M. They simulated miniature excitatory post- et al. Evidence for ectopic neurotransmission at a neuronal synaptic currents (mEPSCs) by imitating synapse. Science 309, 446–451 (2005) 664 | SEPTEMBER 2005 | VOLUME 6 www.nature.com/reviews/neuro.
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