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Received January 27, 2005
Revised February 23, 2005
Accepted after revision February 23, 2005
1 Centre for Integrative Physiology, University of Edinburgh, UK
2 INSERM 583
3 Max Planck Institute of Psychiatry,Munich, Germany
* To whom correspondence should be addressed. E-mail: mike.ludwig{at}ed.ac.uk.
Magnocellular neurons of the hypothalamus release vasopressin and oxytocin from their dendrites and soma. Using a combination of electrophysiology, microdialysis, in vitro explants, and radioimmunoassay we assessed the involvement of intracellular Ca2+ stores in the regulation of dendritic vasopressin release. Thapsigargin and cyclopiazonic acid, which mobilize Ca2+ from intracellular stores of the endoplasmic reticulum, evoked vasopressin release from dendrites and somata of magnocellular neurons in the supraoptic nucleus. Thapsigargin also produced a dramatic potentiation of dendritic vasopressin release evoked by osmotic or high potassium stimulation. This effect is long-lasting, time-dependent, and is specific to thapsigargin as caffeine and ryanodine had no effect. Furthermore, antidromic activation of electrical activity in the cell bodies released vasopressin from dendrites only after thapsigargin pre-treatment. Thus, exposure to Ca2+ mobilizers such as thapsigargin or cyclopiazonic acid primes the releasable pool of vasopressin in the dendrites, so that release can subsequently be evoked by electrical and depolarisation-dependent activation. Although vasopressin is effective in inducing dendritic vasopressin release, it is ineffective in producing priming.
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