ABSTRACT
In 1966 Pearse first described cytochemical and ultrastructural properties which were shared by several apparently disparate cell series in the body – initially adrenomedullary chromaffin cells, enterochromaffin cells, the corticotroph, the melanotroph, the pancreatic islet B cell and the thyroid C cell. Pearse later proposed the generic name APUD for these cells from the initial letters of their common cytochemical characteristics, which include amine precursor uptake and decarboxylase activity within the cells.1 Since that time, the list of APUD cells has expanded enormously. The structural and chemical similarity of APUD cells to neurons suggested a neural crest origin. Indeed, APUD cells of the adrenal medulla, melanocytes, thyroid, gastrointestinal tract and carotid body are of principally neuroectodermal lineage, and the ultrastructural similarity is true for all APUD cells. Pearse considered these cells as ‘neuroendocrine’ programmed cells derived from determined precursors arising in the embryonic epiblast, or in one of its principal early descendants. They are conceived as constituting a diffuse neuroendocrine system (DNES), which may be regarded as a third division of the nervous system, products of which suppress, amplify or modulate the activities of the other two divisions. 2
The DNES is divided into central and peripheral divisions, the first of which contains the cells of the hypothalamo-pituitary axis and the pineal gland, while the cells of the second division are primarily located in the gastrointestinal tract and pancreas, where they comprise the gastro-entero-pancreatic endocrine cells. However, APUD
cells are actually distributed throughout the body, where they are all prone to both hyperplasia and neoplasia, and more recent concepts have tended to decrease the emphasis on a truly discrete and distinct neuroendocrine ‘network’, and also on their presumed embryological commonality.
