Vasopressin-induced calcium signaling in cultured cortical neurons

Son, Michael C.; Brinton, Roberta Dı́az

doi:10.1016/s0006-8993(98)00185-1

Cited by 20 publications

(6 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The lack of response to AVP in cerebrocortical interneurons is in contrast to the increase in [Ca 2ϩ ] i reported by Son and Brinton (1998) in neuronal cultures prepared in almost the same manner as in the present study, with the exception that they were not kept in culture for sufficiently long time to mature (Schousboe and Hertz, 1987). This discrepancy is consistent with the well established ontogenetically transient nature of AVP receptor expres-sion and immunoreactivity in several brain regions (Danilova and Chernigovskaia, 1989;Delville et al, 1994;Iqbal and Jacobson, 1995;Kato et al, 1995;Wang et al, 1997;Panayotacopoulou et al, 2000).…”

Section: Discussionsupporting

confidence: 84%

“…In the present work we have shown that AVP potently increases [Ca 2ϩ ] i in cerebrocortical astrocytes by stimulation of V1b/V3 receptors, whereas AVP had no effect on cultured cortical interneurons. The latter finding is in disagreement with a report by Son and Brinton (1998). These authors, however, cultured fetal neurons for only two days and thus used a very immature preparation.…”

contrasting

confidence: 70%

See 1 more Smart Citation

Vasopressin increases [Ca2+]i in differentiated astrocytes by activation of V1b/V3 receptors but has no effect in mature cortical neurons

2000

View full text Add to dashboard Cite

Vasopressin (AVP) plays an important role in regulation of astrocytic, but not neuronal, water content and cell volume during hydro‐osmotic challenge. To investigate the intracellular mechanism(s) signaling this response, [Ca2+]i was measured fluorometrically in cultured cerebrocortical astrocytes and neurons, obtained from neonatal and fetal mouse brains, and matured during the culturing period. In astrocytes, [Ca2+]i increased with an EC50 of between 10−10 and 10−9 M AVP, the maximum increase was ≈100 nM, and the response was independent of extracellular Ca2+, identifying the receptor as being of the V1b/V3 subtype. In contrast, AVP had no effect on [Ca2+]i in cortical neurons. This cellular difference is consistent with the ability of AVP to increase water permeability in astrocytes but not in neurons. J. Neurosci. Res. 60:761–766, 2000. © 2000 Wiley‐Liss, Inc.

show abstract

Section: Discussionsupporting

confidence: 84%

contrasting

confidence: 70%

Vasopressin increases [Ca2+]i in differentiated astrocytes by activation of V1b/V3 receptors but has no effect in mature cortical neurons

2000

View full text Add to dashboard Cite

show abstract

“…In cultured hippocampal neurones, absence of extracellular Ca 2+ prevented the [Ca 2+ ] i rise induced by the V 1a agonist [Phe 2 , Orn 8 ]‐vasotocin, but not phosphatidylinositol hydrolysis (36). Similarly, in cultured cortical neurones, this V 1a agonist activated the phosphatidylinositol transduction pathway and induced a [Ca 2+ ] i increase via Ca 2+ influx through L‐type voltage‐dependent channels (37). These authors later showed that V 1a receptor activation regulates Ca 2+ influx through L‐type channels via a PKC‐dependent mechanism (38).…”

Section: Discussionmentioning

confidence: 99%

Intracellular Calcium Increase and Somatodendritic Vasopressin Release by Vasopressin Receptor Agonists in the Rat Supraoptic Nucleus: Involvement of Multiple Intracellular Transduction Signals

Sabatier

Shibuya²,

Dayanithi

2004

J Neuroendocrinology

View full text Add to dashboard Cite

Vasopressin neurones of the supraoptic nucleus are autoregulated by vasopressin released from their soma and dendrites. Vasopressin binds to specific autoreceptors to trigger an influx of Ca(2+), and this response involves both phospholipase C (PLC) and adenylate cyclase (AC) pathways that, in the periphery, are activated by V(1) (V(1a) and V(1b))- and V(2)-type receptors. To investigate the pathways involved in the [Ca(2+)](i) response, [Ca(2+)](i) measurements were made on freshly dissociated neurones using Fura-2 microspectrofluorimetry, and vasopressin release was measured from isolated supraoptic nuclei. The [Ca(2+)](i) increase and vasopressin release induced by the V(1a) agonist were strongly inhibited by a PLC blocker, an IP(3) receptor antagonist, and a PKC blocker. An AC inhibitor did not affect the V(1a) response, while PKA inhibitors significantly reduced the V(1a)-induced [Ca(2+)](i) and release responses. The [Ca(2+)](i) increase and vasopressin release elicited by the V(2) agonist were attenuated not only by AC pathway blockers, but also by PLC inhibitors. Surprisingly, the V(1b) agonist showed no [Ca(2+)](i) or vasopressin release response. In conclusion, the V(1a) agonist activates both PLC and AC pathway, confirming the functional expression of a V(1a) vasopressin receptor on vasopressin neurones. The V(2) agonist activation of both PLC and AC pathways could result from an action on the PLC-linked unknown receptor, and/or the AC-linked dual angiotensin II-vasopressin receptor.

show abstract

“…In the present work, [Ca 2+ ] i responses induced by F‐180 were also abolished in a free Ca 2+ buffer, suggesting the involvement of a Ca 2+ influx but not excluding an additional participation of Ca 2+ from internal stores, as has been previously demonstrated for AVP (Dayanithi et al 1996; Sabatier et al 1997). In cultured hippocampal (Brinton et al 1994) and cortical (Son & Brinton, 1998) neurones, the absence of Ca 2+ in the extracellular medium has been shown to abolish the rise in [Ca 2+ ] i induced by a V 1 vasopressin receptor agonist, but the inositol‐1‐phosphate formation persisted. These studies indicate that the absence of extracellular Ca 2+ does not affect the binding characteristics of the V 1 vasopressin receptor.…”

Section: Discussionmentioning

confidence: 99%

V_1a‐ and V₂‐type vasopressin receptors mediate vasopressin‐induced Ca²⁺ responses in isolated rat supraoptic neurones

Gouzènes

Sabatier

Richard

et al. 1999

The Journal of Physiology

View full text Add to dashboard Cite

The pharmacological profile of receptors activated by vasopressin (AVP) in freshly dissociated supraoptic magnocellular neurones was investigated using specific V1a‐ and V2‐type AVP receptor agonists and antagonists. In 97 % of AVP‐responding neurones (1–3000 nm) V1a or V2 receptor type agonists (F‐180 and dDAVP, respectively) elicited dose‐dependent [Ca2+]i transients that were suppressed by removal of external Ca2+. The [Ca2+]i response induced by 1 μm F‐180 or dDAVP was selectively blocked by 10 nm of V1a and V2 antagonists (SR 49059 and SR 121463A, respectively). The response to V1a agonist was maintained in the presence of the V2 antagonist, and the V2 agonist‐induced response persisted in the presence of the V1a antagonist. The [Ca2+]i response induced by 1 μm AVP was partially (61 %) blocked by 10 nm SR 121463A. This blockade was increased by a further 31 % with the addition of 10 nm SR 49059. Similarly, the AVP‐induced response was partially (47 %) decreased by SR 49059, and a further inhibition of 33 % was achieved in the presence of SR 121463A. We demonstrate that AVP acts on the magnocellular neurones via two distinct types of AVP receptors that exhibit the pharmacological profiles of V1a and V2 types. However, since V2 receptor mRNA is not expressed in the supraoptic nucleus (SON), and since V1b receptor transcripts are observed in the SON, we propose that the V2 receptor agonist and antagonist act on a ‘V2‐like’ receptor or a new type of AVP receptor that remains to be elucidated. The possibility that V2 ligands act on the V1b receptor cannot be excluded.

show abstract

Vasopressin-induced calcium signaling in cultured cortical neurons

Cited by 20 publications

References 56 publications

Vasopressin increases [Ca2+]i in differentiated astrocytes by activation of V1b/V3 receptors but has no effect in mature cortical neurons

Vasopressin increases [Ca2+]i in differentiated astrocytes by activation of V1b/V3 receptors but has no effect in mature cortical neurons

Intracellular Calcium Increase and Somatodendritic Vasopressin Release by Vasopressin Receptor Agonists in the Rat Supraoptic Nucleus: Involvement of Multiple Intracellular Transduction Signals

V_1a‐ and V₂‐type vasopressin receptors mediate vasopressin‐induced Ca²⁺ responses in isolated rat supraoptic neurones

Contact Info

Product

Resources

About

Vasopressin-induced calcium signaling in cultured cortical neurons

Cited by 20 publications

References 56 publications

Vasopressin increases [Ca2+]i in differentiated astrocytes by activation of V1b/V3 receptors but has no effect in mature cortical neurons

Vasopressin increases [Ca2+]i in differentiated astrocytes by activation of V1b/V3 receptors but has no effect in mature cortical neurons

Intracellular Calcium Increase and Somatodendritic Vasopressin Release by Vasopressin Receptor Agonists in the Rat Supraoptic Nucleus: Involvement of Multiple Intracellular Transduction Signals

V1a‐ and V2‐type vasopressin receptors mediate vasopressin‐induced Ca2+ responses in isolated rat supraoptic neurones

Contact Info

Product

Resources

About

V_1a‐ and V₂‐type vasopressin receptors mediate vasopressin‐induced Ca²⁺ responses in isolated rat supraoptic neurones