Abstract
There is limited information on the regeneration of the enteric nervous system (ENS) following major reconstruction of the digestive tract. We have studied ENS regeneration in the sea cucumber Holothuria glaberrima which undergoes an organogenic process forming a new digestive tract at the tip of the mesentery. Our results show that (1) a degeneration of nerve fibers occurs early in the regeneration process, prior to eventual regeneration; (2) nerve fibers that innervate the regenerating intestine are of extrinsic and intrinsic origin; (3) innervation by extrinsic fibers occurs in a gradient that begins in the proximal area of the regenerate; (4) late events include the appearance of nerve fibers that project from the serosa into the connective tissue and of nerve bundles in the mesothelial layer; (5) neurons and neuroendocrine cells appear early following the formation of the epithelial layers. Our results provide not only a comparative biological approach to study ENS regeneration but also an alternative point of view for the study of enteric neuropathologies and for the innervation of organs made in vitro.
Highlights
The enteric nervous system (ENS) constitutes the ensemble of neural tissue that innervates the gastrointestinal tract
To understand ENS regeneration in H. glaberrima, it is necessary to describe the organization of the normal holothurian ENS
Rather than viewing the antibodies as markers for the presence of antigens corresponding to the holothurian homologs, we have used them as markers of particular cell and fiber populations to be able to follow their regeneration during the formation of a new intestine
Summary
The enteric nervous system (ENS) constitutes the ensemble of neural tissue that innervates the gastrointestinal tract. The ENS components are arranged into plexi that are located in various areas of the digestive tract. These plexi are interconnected networks made of neurons, their axons and enteric glial cells (Furness 2006). Problems with ENS function can cause several neuropathies both neurodegenerative and inflammatory (Neunlist et al 2012; Knowles et al 2013). Some of these neuropathies are caused by the loss of ENS components and the resulting loss of ENS function
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