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Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2015.166 Figure 4 Neuropathic–neuroplastic alterations in human and experimental chronic pancreatitis Figure 4 | Neuropathic–neuroplastic alterations in human and experimental chronic pancreatitis. Neurophysiological and neuroimaging studies in the past decade detected striking differences in the functionality of the peripheral nervous system, in the excitability of central neurons and the cortical structure among patients with chronic pancreatitis as opposed to healthy individuals. In animal models of chronic pancreatitis and pancreatic cancer, ion channels that are typically found on sensory neurons (TRPV1, TRPA1) or nociceptive neuropeptides like CGRP have been reported to be overexpressed within the pancreas-innervating DRG.11,62,63,104 Furthermore, these DRG neurons were also shown to upregulate the expression of NGF, TRKB neurotrophin receptor, the neurotrophic factor neurturin and its receptor GFRα2 during the course of chronic pancreatitis.11,20,62,63,104 Data represented in the blue dotted circle are from experimental mouse models. Abbreviations: CGRP, calcitonin-gene-related peptide; EEG, electroencephalography; GFRα2, glial cell line derived neurotrophic factor family receptor alpha 2; NGF, nerve growth factor; TRKB, tyrosine receptor kinase B; TRPA1, transient receptor potential member A1; TRPV1, transient receptor potential vanilloid 1. Demir, I. E. et al. (2015) Neural plasticity in pancreatitis and pancreatic cancer Nat. Rev. Gastroenterol. Hepatol. doi:10.1038/nrgastro.2015.166