The role of microvesicles in buffering [Ca2+]i in the neurohypophysis.

Abstract

It is well established that hormone release from neurosecretory nerve terminals is triggered by an increase of the cytoplasmic ionized calcium concentration which occurs after the arrival of action potentials1. For the neurosecretory nerve terminals to recover their basal Ca2+ concentration, the calcium which has entered during depolarization must be extruded and/or accumulated in subcellular organelles or bound to some cytoplasmic proteins. Neurosecretory nerve endings are characterized by the presence of hormone-containing granules and microvesicles (earlier referred to as ‘synaptoid’ vesicles). The role of these microvesicles has been the subject of debate and has recently been reviewed2. One of the most attractive hypotheses has been that these organelles represent the retrieved membrane of the granule after exocytosis. However, on stimulation of hormone release, the number of microvesicles does not increase, suggesting that they do not participate in the endocytotic process3. Using stereology as a quantifying method, we recently demonstrated a redistribution of microvesicles towards the release site during potassium-stimulated hormone release3. It is thus possible that microvesicles in neurosecretory nerve terminals might function as calcium accumulating organelles as suggested for the coated vesicles isolated from the cerebral cortex4,5. We report here that a microvesicle-containing microsomal fraction isolated from neurosecretosomes (isolated neurosecretory nerve terminals) possesses an ATP-dependent calcium transporting system. This system enables the fraction to accumulate calcium ions when the external ionized calcium concentration is <1 µM, which is in the physiological range.