Intracellular Control of Exocytosis in Chromaffin Cells

  • Alan Morgan
  • Isabelle Cenci de Bello
  • Ulrich Weller
  • J. Oliver Dolly
  • Robert D. Burgoyne


Chromaffin cells are endocrine cells of the adrenal medulla which synthesize large quantities of adrenaline and noradrenaline and store these, along with a cocktail of other compounds including bioactive peptides, within membrane-enclosed secretory vesicles known as chromaffin granules. In situations of stress, acetylcholine is released from splanchnic nerve terminals innervating the adrenal medulla and this in turn causes the chromaffin granule membranes to fuse with the plasma membrane of the cell, thereby releasing the granule contents into the blood to effect the ‘fight or flight response’. Acetylcholine, then, is the physiological stimulus resulting in the exocytotic secretion of catecholamines from chromaffin cells. Acetylcholine can activate nicotinic and muscarinic receptors; and chromaffin cells possess both types of receptor. Selective activation of either nicotinic or muscarinic receptors results in a similar increase in cytosolic Ca2+ concentration (long recognised as the major signal leading to exocytosis in this and many other secretory cell types), but only nicotinic receptor agonists elicit exocytosis, muscarinic agonists being ineffective.l,2 This paradox can be explained by the source of the increased cytosolic Ca2+. Nicotinic receptor activation depolarises the plasma membrane causing entry of extracellular Ca2+ through voltage-dependent Ca2+ channels, whereas muscarinic receptor activation causes IP3 generation and subsequent release of Ca2+ from intracellular stores.3 Thus, exocytosis requires entry of extracellular Ca2+–intracellular Ca2+ mobilization is ineffective. That this is the case is evidenced by the observation that nicotinic agonists (and indeed all secretagogues so far tested) fail to elicit a secretory response in the absence of extracellular Ca2+.3 Although no direct evidence is available to explain the crucial nature of extracellular Ca2+ entry in exocytosis, it is likely that the opening of plasma membrane channels would lead to a very high level of Ca2+ immediately beneath the plasma membrane—the very region in which the process of exocytotic membrane fusion occurs. Indeed, it has been calculated that the influx of Ca2+ through such channels could raise intracellular Ca2+ levels within a few nanometres of the plasma membrane to as high as 100µM.4


Chromaffin Cell Botulinum Neurotoxin Tetanus Toxin Arachidonic Acid Release Adrenal Chromaffin Cell 
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Copyright information

© Springer Science+Business Media New York 1993

Authors and Affiliations

  • Alan Morgan
    • 1
  • Isabelle Cenci de Bello
    • 2
  • Ulrich Weller
    • 3
  • J. Oliver Dolly
    • 2
  • Robert D. Burgoyne
    • 1
  1. 1.The Physiological LaboratoryUniversity of LiverpoolLiverpoolUK
  2. 2.Biochemistry Dept, Imperial CollegeSouth KensingtonLondonUK
  3. 3.Abteilung fur Neuropsychopharmakologie der Freien UniversitatBerlinGermany

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