Enteric Nervous System Abnormalities in Ulcerative Colitis

Ulcerative colitis (UC) is a chronic non-specific inflammatory disease affecting the mucosa and the submucosa of the colon, and is characterized by alterations of gut functions which influence the clinical symptoms (Fiocchi, 1998; Reddy et al., 1991; Spriggs et al., 1951). Although reports showed morpho-functional abnormalities of the enteric nervous system in UC patients, the available literature is still heterogeneous and confusing. UC-related intestinal inflammation causes structural and functional changes to the enteric nervous system and its cellular components (neurons and glial cells), which could be directly related to the development of the disease and its associated symptoms (Geboes & Collins, 1998; Lakhan & Kirchgessner, 2010; Lomax et al., 2005; Villanacci et al., 2008). UC-related alteration in the enteric nervous system can be categorised into two groups: a) the alterations that occur in the structural morphology of the system, and b) those that occur in the level of enteric transmitters released by neurons and glial cells (Lakhan & Kirchgessner, 2010). Routine pathology of UC reports describe: 1) hypertrophy, hyperplasia and axonal damage of nerve fibres (Cook & Dixon, 1973; Geboes, 1993); 2) a normal aspect, hypertrophy, hyperplasia or damage of neuronal cell bodies (Belai et al., 1997; Siemers & Dobbins, 1974; Strobach et al., 1990); 3) glial cells hyperplasia (Antonius et al., 1960); 4) a variable increase of glial cells number (Geboes et al., 1992; Koretz et al., 1987); and 5) ganglioneuritis (Ohlsson et al., 2007). Besides structural changes, disruption in the function of neurons and glial cells is reported in patients with UC: defective neuronal control of epithelial secretion, increased excitability of enteric neurons, alteration in synaptic transmission, and variablility in the expression of neuronal and glial-derived factors (vasoactive intestinal peptide, inducible nitric oxide synthase and other mediators in neuronal cell bodies; S100B protein, glial fibrillary acidic protein and other factors in glial cells) (Lomax et al., 2005). The aim of this chapter is to illustrate the new insights into the pathophysiology of UC, providing an exhaustive overview of the current knowledge of the role of the enteric nervous system during gut inflammation. Initially, we describe the morphology and the basic physiological functions of the enteric nervous system and its cellular components, neurons and glial cells, respectively. Then, a more extensive part is dedicated to the modifications of the enteric nervous system in UC. Besides the well documented role of enteric neurons, attention is also focused on the