Decoding the Neuronal Tower of Babel

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Science  26 Oct 2012:
Vol. 338, Issue 6106, pp. 482-483
DOI: 10.1126/science.1230338

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Individual neurons in the mammalian central nervous system communicate with their downstream targets by means of subcellular specializations in their axon. Arranged like pearls on a necklace, these presynaptic terminals enable the rapid release of neurotransmitter in response to an electrical action-potential wave front that travels from the cell body to the far reaches of the axon. A single axon may contact hundreds of downstream targets, including numerous distinct cell types. Though separated by only a few micrometers, each of these presynaptic release sites is often tuned to the particular cell type it innervates such that transmission may be robust onto one particular cell type yet weak at another, despite all terminals sensing the same action-potential waveform (1). This arrangement allows different terminals in the axon to behave independently and “translate” presynaptic action potentials into their own unique chemical language to effect both short- and long-term synaptic transmission and plasticity (2, 3). Whether elements in the presynaptic terminal, postsynaptic membrane, or transynaptic proteins dictate this differential synaptic processing has been unclear. On page 536 in this issue, Sylwestrak and Ghosh (4) show that postsynaptic expression of the extracellular leucine-rich repeat fibronectin-containing 1 (Elfn1) plays an important role in establishing such target-specific differential transmission.