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1 Centre for Integrative Physiology, University of Edinburgh, Edinburgh EH8 9XD, UK
2 Max Planck Institute of Psychiatry, 80804 Munich, Germany
3 INSERM 583, University of Montpellier II, F-34095 Montpellier Cedex 5, France
Magnocellular neurones 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 neurones 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 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 pretreatment. 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 depolarization-dependent activation. Vasopressin itself is effective in inducing dendritic vasopressin release, but it is ineffective in producing priming.
(Received 27 January 2005;
accepted after revision 23 February 2005;
first published online 24 February 2005)
Corresponding author M. Ludwig: Centre for Integrative Physiology, University of Edinburgh, George Square, Edinburgh EH8 9XD, UK. Email: mike.ludwig{at}ed.ac.uk
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