Endocrine Abstracts

Although the notion of paracrine and autocrine signalling was already suggested more than 100 years ago, its full recognition dates from the last 30 years. Paracrine communication and autocrine loops have been shown to operate in all hormonal cell types and in folliculo-stellate cells and other non-hormonal cells during fetal and postnatal development and adulthood. More than 100 compounds have been identified that have, or may have, paracrine or autocrine actions, including the neurotransmitters acetylcholine and γ-aminobutyric acid, neuropeptides, growth factors, cytokines, annexin-1, follistatin, hormones, nitric oxide, purines, retinoids and fatty acid derivatives. Connective tissue cells, endothelial cells and vascular pericytes may contribute to paracrinicity by delivering growth factors, heparan sulphate proteoglycans and proteases and basement membranes may influence paracrine signalling through the binding of signalling molecules to heparan sulphate proteoglycans. The present symposium will highlight some of the more recent achievements and growing concepts concerning the integrated action of these factors in maintaining adaptation and homeostasis of pituitary function when hormonal outputs need to be adapted to changing demands of the organism, such as during reproduction, stress, inflammation, starvation and circadian rhythms. A second focus will be the growing notion that paracrine/autocrine actions are highly context-dependent and that specificity and selectivity in these interactions may rely on microanatomical specialisations, functional compartmentalisation in receptor–ligand distribution and the non-equilibrium dynamics of the receptor–ligand interactions in the loops.