GSBS Student Publications

Student Author(s)

James McNally

GSBS Program


UMMS Affiliation

Department of Physiology



Document Type


Medical Subject Headings

Animals; Calcium; Chromaffin Cells; Dopamine; Electric Capacitance; Exocytosis; Membrane Potentials; Mice; Neurons; Patch-Clamp Techniques; Pituitary Gland, Posterior


Life Sciences | Medicine and Health Sciences | Neuroscience and Neurobiology


Recently, highly localized Ca(2+) release events, similar to Ca(2+) sparks in muscle, have been observed in neuronal preparations. Specifically, in murine neurohypophysial terminals (NHT), these events, termed Ca(2+) syntillas, emanate from a ryanodine-sensitive intracellular Ca(2+) pool and increase in frequency with depolarization in the absence of Ca(2+) influx. Despite such knowledge of the nature of these Ca(2+) release events, their physiological role in this system has yet to be defined. Such localized Ca(2+) release events, if they occur in the precise location of the final exocytotic event(s), may directly trigger exocytosis. However, directly addressing this hypothesis has not been possible, since no method capable of visualizing individual release events in these CNS terminals has been available. Here, we have adapted an amperometric method for studying vesicle fusion to this system which relies on loading the secretory granules with the false transmitter dopamine, thus allowing, for the first time, the recording of individual exocytotic events from peptidergic NHT. Simultaneous use of this technique along with high-speed Ca(2+) imaging has enabled us to establish that spontaneous neuropeptide release and Ca(2+) syntillas do not display any observable temporal or spatial correlation, confirming similar findings in chromaffin cells. Although these results indicate that syntillas do not play a direct role in eliciting spontaneous release, they do not rule out indirect modulatory effects of syntillas on secretion.

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Citation: J Neurosci. 2009 Nov 11;29(45):14120-6. Link to article on publisher's site

Related Resources

Link to Article in PubMed



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