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The Journal of Neuroscience, August 4, 2004, 24(31):6904-6911; doi:10.1523/JNEUROSCI.1978-04.2004

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Development/Plasticity/Repair
Synaptic Strengthening Mediated by Bone Morphogenetic Protein-Dependent Retrograde Signaling in the Drosophila CNS

Richard A. Baines

Neuroscience Group, Department of Biological Sciences, University of Warwick, Coventry, CV4 7AL, United Kingdom

Retrograde signaling is an essential component of synaptic development and physiology. Previous studies show that bone morphogenetic protein (BMP)-dependent retrograde signaling is required for the proper development of the neuromuscular junction (NMJ) in Drosophila. These studies, moreover, raised the significant possibility that the development of central motor circuitry might similarly be reliant on such signaling. To test this hypothesis, retrograde signaling between postsynaptic motoneurons and their presynaptic interneurons is examined. Postsynaptic expression of an adenylate cyclase encoded by rutabaga (rut), is sufficient to strengthen synaptic transmission at these identified central synapses. Results are presented to show that the underlying mechanism is dependent on BMP retrograde signaling. Thus, presynaptic expression of an activated TGF- receptor, thickvien (tkv), or postsynaptic expression of a TGF- ligand, glass-bottom boat (gbb), is sufficient to phenocopy strengthening of synaptic transmission. In the absence of gbb, endogenous synaptic transmission is significantly weakened and, moreover, postsynaptic overexpression of rut is unable to potentiate synaptic function. Potentiation of presynaptic neurotransmitter release, mediated by increased postsynaptic expression of gbb, is dependent on normal cholinergic activity, indicative that either the secretion of this retrograde signal, or its transduction, is activity dependent. Thus, in addition to the development of the NMJ and expression of myoactive FMRFamide-like peptides in specific central neurons, the results of the present study indicate that this retrograde signaling cascade also integrates the development and function of central motor circuitry that controls movement in Drosophila larvae.

Key words: aCC; Gbb; neural activity; retrograde signaling; RP2; synaptic development

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Received March 29, 2004; revised June 23, 2004; accepted June 23, 2004.

This article has been cited by other articles:

				L. G. Fradkin, R. A. Baines, M. C. van der Plas, and J. N. Noordermeer The Dystrophin Dp186 Isoform Regulates Neurotransmitter Release at a Central Synapse in Drosophila J. Neurosci., May 7, 2008; 28(19): 5105 - 5114. [Abstract] [Full Text] [PDF]

				M. Sun, M. J. Thomas, R. Herder, M. L. Bofenkamp, S. B. Selleck, and M. B. O'Connor Presynaptic Contributions of Chordin to Hippocampal Plasticity and Spatial Learning J. Neurosci., July 18, 2007; 27(29): 7740 - 7750. [Abstract] [Full Text] [PDF]

				M. C. van der Plas, G. S. K. Pilgram, J. J. Plomp, A. de Jong, L. G. Fradkin, and J. N. Noordermeer Dystrophin Is Required for Appropriate Retrograde Control of Neurotransmitter Release at the Drosophila Neuromuscular Junction J. Neurosci., January 4, 2006; 26(1): 333 - 344. [Abstract] [Full Text] [PDF]

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