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Comparative Study
. 2005 Apr 15;564(Pt 2):515-22.
doi: 10.1113/jphysiol.2005.083931. Epub 2005 Feb 24.

Regulation of activity-dependent dendritic vasopressin release from rat supraoptic neurones

Mike Ludwig  1 , Philip M Bull, Vicky A Tobin, Nancy Sabatier, Rainer Landgraf, Govindan Dayanithi, Gareth Leng
Affiliations
Comparative Study

Regulation of activity-dependent dendritic vasopressin release from rat supraoptic neurones

Mike Ludwig et al. J Physiol. .

Abstract

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 Ca(2+) stores in the regulation of dendritic vasopressin release. Thapsigargin and cyclopiazonic acid, which mobilize Ca(2+) 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 Ca(2+) 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.

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Figures

Figure 1
Figure 1. Vasopressin release in the SON
A, release after intraperitoneal (i.p.) injection of hypertonic saline (HS) after dialysis of one SON with thapsigargin (TG, 200 nm, given during the second 30-min dialysis interval) or control solution. n = 6, *P < 0.05, analysis of variance (ANOVA). B, vasopressin measured in the plasma in the same experiments as A. *P < 0.05, compared to basal. C, vasopressin release in the SON before (black columns) and in response to electrical stimulation of the neural stalk (white columns) or thapsigargin (grey column) and electrical stimulation after exposure of one SON to thapsigargin (hatched column). Data are means ± s.e.m., n = 8, *P < 0.05, **P < 0.01, compared to controls, t tests.
Figure 2
Figure 2. Effects of thapsigargin (TG) on vasopressin release in vitro
A and C, repeated stimulation with high-K+ solutions results in repeatable responses in vasopressin release from isolated neural lobes (A) and SON (C). B and D, vasopressin release from isolated SON (D), and neural lobes (B) before and after thapsigargin (TG). E, release from the SON only, evoked by depolarization with high-K+ solutions, was strongly potentiated by thapsigargin; the potentiation was long-lasting and time dependent. F, release from the SON only, evoked by depolarization with high-K+ solutions, was strongly potentiated by thapsigargin, but not by caffeine or ryanodine. Data are means ± s.e.m., n = 4 per group for each experiment, *P < 0.05, t tests.
Figure 3
Figure 3. Effects of cyclopiazonic acid (CPA) on vasopressin release in vitro
Vasopressin release from isolated SON evoked by depolarization with high-K+ solutions was strongly potentiated by CPA (n = 7). The potentiation was similar to the potentiation seen with thapsigargin (Fig. 2D).
Figure 4
Figure 4. Effects of vasopressin agonists on vasopressin release in vitro
A, application of a mixture of V1a and V2 (1 μm) agonists significantly increased vasopressin release from the isolated SON in vitro, but did not potentiate subsequent K+-induced release. B, this response was only partially blocked by preapplication of a mixture of Ca2+-channel blockers. C, however, pretreatment with Ca2+-channel blockers blocked the high-K+ evoked response in vasopressin release. Data are means ± s.e.m., t tests, n = 4 per group for each experiment.
Figure 5
Figure 5. Effects of thapsigargin (TG) on the electrical activity of vasopressin cells
A, recording of the electrical activity of a phasically firing vasopressin neurone showing an increase in the activity induced by microdialysis administration (retrodialysis) of thapsigargin (TG, 200 nm) onto the SON. B and C, changes in activity quotient (B) but not intraburst activity (C) after TG (P < 0.05, n = 6). D, continuously active vasopressin neurones were not affected by thapsigargin. n = 8, Data are means ± s.e.m., *P < 0.05, t tests.
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