Effects of nerve injury and segmental regeneration on the cellular correlates of neural morphallaxis

✍ Scribed by Veronica G. Martinez; Josiah M.B. Manson; Mark J. Zoran

• Publisher: John Wiley and Sons
• Year: 2008
• Tongue: English
• Weight: 254 KB
• Volume: 310B
• Category: Article
• ISSN: 1552-5007
• DOI: 10.1002/jez.b.21224

✦ Synopsis

Abstract

Functional recovery of neural networks after injury requires a series of signaling events similar to the embryonic processes that governed initial network construction. Neural morphallaxis, a form of nervous system regeneration, involves reorganization of adult neural connectivity patterns. Neural morphallaxis in the worm, Lumbriculus variegatus, occurs during asexual reproduction and segmental regeneration, as body fragments acquire new positional identities along the anterior–posterior axis. Ectopic head (EH) formation, induced by ventral nerve cord lesion, generated morphallactic plasticity including the reorganization of interneuronal sensory fields and the induction of a molecular marker of neural morphallaxis. Morphallactic changes occurred only in segments posterior to an EH. Neither EH formation, nor neural morphallaxis was observed after dorsal body lesions, indicating a role for nerve cord injury in morphallaxis induction. Furthermore, a hierarchical system of neurobehavioral control was observed, where anterior heads were dominant and an EH controlled body movements only in the absence of the anterior head. Both suppression of segmental regeneration and blockade of asexual fission, after treatment with boric acid, disrupted the maintenance of neural morphallaxis, but did not block its induction. Therefore, segmental regeneration (i.e., epimorphosis) may not be required for the induction of morphallactic remodeling of neural networks. However, on‐going epimorphosis appears necessary for the long‐term consolidation of cellular and molecular mechanisms underlying the morphallaxis of neural circuitry. J. Exp. Zool. (Mol. Dev. Evol.) 310B:520–533, 2008. © 2008 Wiley‐Liss, Inc.