The Experts below are selected from a list of 189 Experts worldwide ranked by ideXlab platform
Jean-marc Mienville - One of the best experts on this subject based on the ideXlab platform.
-
Pituicyte modulation of neurohormone output
Glia, 2009Co-Authors: Lia Rosso, Jean-marc MienvilleAbstract:Pituicytes have long been suspected to play a role in the regulation of neurohypophysial hormone output. This role has been mainly ascribed to morphological changes in these cells and subsequent modifications of their tight structural relationships with surrounding nerve terminals and capillaries. These entirely reversible changes are brought about by physiological states such as parturition, lactation, or dehydration, and it was inferred that they should facilitate neurohormone output, based on concerted analyses of in vitro, in situ, and ex vivo experiments. Pituicyte stellation, the in vitro counterpart of these morphological changes, can be induced by β-adrenergic or A1-adenosine receptor activation, and appears to result from inhibition of the small GTPase RhoA. Actin depolymerization is the key event allowing stellation. Vasopressin and oxytocin reverse stellation and return Pituicytes to their basal shape by activating Cdc42, another small GTPase that reorganizes the actin cytoskeleton in a cortical position. Adenosine and neurohormones also have opposite actions on the efflux of taurine, a local messenger that is released by Pituicytes in hypotonic conditions and accordingly inhibits vasopressin output from axon terminals. As adenosine is likely generated from endogenous ATP co-released with neurohormones and broken down by local ectoATPases, these data suggest a subtle balance between a positive and a negative feedback on vasopressin output operated, respectively, by adenosine and vasopressin to maintain hydromineral homeostasis. A theoretical scenario is presented to account for the putative sequence of Pituicyte-related events following disturbance of the hydromineral system. © 2008 Wiley-Liss, Inc.
-
Pituicyte stellation is prevented by RhoA-or Cdc42-dependent actin polymerization.
Cellular and Molecular Neurobiology, 2007Co-Authors: Lia Rosso, Brigitta Peteri-brunbäck, Christophe Deroanne, Ellen Van Obberghen-schilling, Patricia M Pierson, Claire Golfier, Jean-marc MienvilleAbstract:Our aim was to shed light on different steps leading from metabotropic receptor activation to changes in cell shape, such as those that characterize the morphological plasticity of neurohypophysial astrocytes (Pituicytes). Using explant cultures of adult rat Pituicytes, we have previously established that adenosine A1 receptor activation induces stellation via inhibition of RhoA monomeric GTPase and subsequent disruption of actin stress fibers. Here, we rule out RhoA phosphorylation as a mechanism for that inhibition. Rather, our results are more consistent with involvement of a GTPase-activating protein (GAP). siRNA and pull-down experiments suggest that a step downstream of RhoA might involve Cdc42, another GTPase of the Rho family. However, RhoA activation, e.g., in the presence of serum, induces stress fibers, whereas direct Cdc42 activation appears to confine actin within a submembrane - i.e., cortical - network, which also prevents stellation. Therefore, we propose that RhoA may activate Cdc42 in parallel with an effector, such as p160Rho-kinase, that induces and maintains actin stress fibers in a dominant fashion. Rac1 is not involved in the stellation process per se but appears to induce a dendritogenic effect. Ultimately, it may be stated that Pituicyte stellation is inducible upon mere actin depolymerization, and preventable upon actin organization, be it in the form of stress fibers or in a cortical configuration.
-
A2b receptor mediates adenosine inhibition of taurine efflux from Pituicytes
Biology of the cell, 2007Co-Authors: Patricia M Pierson, Brigitta Peteri-brunbäck, Jean-marc Mienville, D.f. Pisani, M.p. Abbracchio, Lia RossoAbstract:Background information. Recent work suggests that part of the control of vasopressin output is mediated by taurine released from Pituicytes, the astroglial cells of the neurohypophysis. Taurine release, in turn, is stimulated by hypotonic conditions and by vasopressin itself. As adenosine is generated from ATP co-released with vasopressin, it appeared important to study its effects on taurine efflux from Pituicytes. Results. We measured radioactive efflux from cultured Pituicytes and whole neurohypophyses pre-loaded with [3H]taurine. Cultured Pituicytes were also used to study adenosine-receptor mRNA expression. Taurine efflux elicited by hypotonic shocks is ∼30–50% smaller in the presence of 10 μM adenosine or 1 μM NECA (5′-N-ethylcarboxamidoadenosine). Both compounds also inhibited basal efflux in a manner that was not immediately reversible. Agonists of the adenosine A1-, A2a- or A3-receptor subtypes have no relevant effect on basal taurine release, and the A1-receptor antagonist DPCPX (8-cyclopentyl-1,3-dipropylxanthine) has no effect on the inhibition of release by NECA. In turn, the A2b-receptor antagonists MRS 1706 {N-(4-acetylphenyl)-2-[4-(2,3,6,7-tetrahydro-2,6-dioxo-1,3-dipropyl-1H-purin-8-yl)phenoxy]acetamide} or alloxazine partially reverse the inhibition of basal or hypotonicity-evoked efflux by NECA. Both A1- and A2b-receptor mRNAs are expressed in Pituicytes, which is consistent with an A1-receptor-mediated effect on cell morphology and an A2b-receptor-mediated effect on taurine release. Forskolin and dibutyryl cAMP mimic the inhibitory effects of purinergics on basal taurine efflux, and the adenylate cyclase inhibitor DDA (2′,5′-dideoxyadenosine) partially reverses the inhibition of the hypotonic response by NECA. Conclusions. Our results suggest that purinergic inhibition of taurine efflux from Pituicytes operates through A2b receptors coupled to intracellular cAMP increase. They point to a possible modulation of neurohypophysial hormone output by endogenous adenosine released in either physiological or pathological situations.
-
Putative physiological significance of vasopressin V1a receptor activation in rat Pituicytes.
Journal of neuroendocrinology, 2004Co-Authors: Lia Rosso, Brigitta Peteri-brunbäck, Jean-marc MienvilleAbstract:Physiological stimuli operative during, for example, dehydration or lactation, induce neurohypophysial astrocytes (Pituicytes) to undergo reversible morphological changes, which in turn may modulate the release of vasopressin and oxytocin. To study the molecular mechanisms of this morphological plasticity, we used primary cultures of rat Pituicytes. During stimulation with adenosine, Pituicytes become stellate, which is characterized by a round, phase-bright soma and complex arborization, implying major cytoskeletal modifications. Following addition of vasopressin or oxytocin, stellate Pituicytes revert to a flat shape. The effects of both hormones are mediated by V(1a) receptor activation, which also induces biphasic Ca(2+) (i) signals in Pituicytes. Stellation reversal requires Ca(2+)-dependent activation of Cdc42, a small GTPase known to impact on the cytoskeleton. V(1a) receptor activation by vasopressin or oxytocin also stimulates [(3)H]taurine efflux from cultured Pituicytes. As taurine inhibits vasopressin output from neurohypophysial terminals, we postulate a negative-feedback mechanism whereby secreted vasopressin limits its own availability. This stop signal might be reinforced by shape changes elicited by vasopressin in Pituicytes. These results support the concept that, during specific physiological states, Pituicyte V(1a) receptor activation modulates the release of neurohypophysial hormones.
-
Vasopressin and oxytocin reverse adenosine-induced Pituicyte stellation via calcium-dependent activation of Cdc42.
The European journal of neuroscience, 2002Co-Authors: Lia Rosso, Brigitta Peteri-brunbäck, Valérie Vouret-craviari, Christophe Deroanne, Ellen Van Obberghen-schilling, Jean-marc MienvilleAbstract:In view of the potential impact of Pituicyte morphology on neurohypophysial hormone secretion, we have studied the mechanisms involved in the shape changes induced by vasopressin (AVP) and oxytocin (OXT) in cultured rat Pituicytes. Pituicytes induced to become stellate in the presence of 10 mM adenosine revert to their nonstellate shape ~20 min after application of AVP or OXT. The IC50 for this effect is 0.1 nM for AVP and 36 nM for OXT. Both agonists induce Ca 2+ signals in Pituicytes, comprised of a transient peak and a plateau phase that is dependent on the presence of extracellular Ca 2+ . The EC50 values of AVP for the transient and sustained responses are 4.5 and 0.1 nM, respectively; corresponding values for OXT are 180 and 107 nM .W e determined pharmacologically that these hormone-induced Ca 2+ signals are mediated by the V1a subtype of vasopressin receptors, similar to what we previously observed for hormone-induced reversal of stellation. Removal of extracellular Ca 2+ or chelation of intracellular Ca 2+ partially prevented AVP from reversing stellation, suggesting a role for Ca 2+ in this event. We previously established that adenosine-induced stellation of Pituicytes occurs via RhoA inhibition. However, pharmacological experiments and pull-down assays presented here show that AVP-induced reversal of stellation does not involve RhoA activation. Rather, AVP was found to induce a time-dependent activation of Cdc42, another small GTPase involved in cytoskeletal plasticity. Activation of Cdc42 by AVP is sensitive to intra- and extracellular Ca 2+ depletion, similar to AVP-induced reversal of stellation. Furthermore, AVP-induced reversal of stellation is blocked by expression of an NWASP fragment known to inhibit endogenous Cdc42.
Lia Rosso - One of the best experts on this subject based on the ideXlab platform.
-
Status: Postprint (Author’s version)
2016Co-Authors: Lia Rosso, Brigitta Peteri-brunbäck, Valérie Vouret-craviari, Christophe Deroanne, Ellen Van ObberghenAbstract:Vasopressin and oxytocin reverse adenosine-induced Pituicyte stellation via calcium-dependent activation of Cdc4
-
Pituicyte modulation of neurohormone output
Glia, 2009Co-Authors: Lia Rosso, Jean-marc MienvilleAbstract:Pituicytes have long been suspected to play a role in the regulation of neurohypophysial hormone output. This role has been mainly ascribed to morphological changes in these cells and subsequent modifications of their tight structural relationships with surrounding nerve terminals and capillaries. These entirely reversible changes are brought about by physiological states such as parturition, lactation, or dehydration, and it was inferred that they should facilitate neurohormone output, based on concerted analyses of in vitro, in situ, and ex vivo experiments. Pituicyte stellation, the in vitro counterpart of these morphological changes, can be induced by β-adrenergic or A1-adenosine receptor activation, and appears to result from inhibition of the small GTPase RhoA. Actin depolymerization is the key event allowing stellation. Vasopressin and oxytocin reverse stellation and return Pituicytes to their basal shape by activating Cdc42, another small GTPase that reorganizes the actin cytoskeleton in a cortical position. Adenosine and neurohormones also have opposite actions on the efflux of taurine, a local messenger that is released by Pituicytes in hypotonic conditions and accordingly inhibits vasopressin output from axon terminals. As adenosine is likely generated from endogenous ATP co-released with neurohormones and broken down by local ectoATPases, these data suggest a subtle balance between a positive and a negative feedback on vasopressin output operated, respectively, by adenosine and vasopressin to maintain hydromineral homeostasis. A theoretical scenario is presented to account for the putative sequence of Pituicyte-related events following disturbance of the hydromineral system. © 2008 Wiley-Liss, Inc.
-
Pituicyte stellation is prevented by RhoA-or Cdc42-dependent actin polymerization.
Cellular and Molecular Neurobiology, 2007Co-Authors: Lia Rosso, Brigitta Peteri-brunbäck, Christophe Deroanne, Ellen Van Obberghen-schilling, Patricia M Pierson, Claire Golfier, Jean-marc MienvilleAbstract:Our aim was to shed light on different steps leading from metabotropic receptor activation to changes in cell shape, such as those that characterize the morphological plasticity of neurohypophysial astrocytes (Pituicytes). Using explant cultures of adult rat Pituicytes, we have previously established that adenosine A1 receptor activation induces stellation via inhibition of RhoA monomeric GTPase and subsequent disruption of actin stress fibers. Here, we rule out RhoA phosphorylation as a mechanism for that inhibition. Rather, our results are more consistent with involvement of a GTPase-activating protein (GAP). siRNA and pull-down experiments suggest that a step downstream of RhoA might involve Cdc42, another GTPase of the Rho family. However, RhoA activation, e.g., in the presence of serum, induces stress fibers, whereas direct Cdc42 activation appears to confine actin within a submembrane - i.e., cortical - network, which also prevents stellation. Therefore, we propose that RhoA may activate Cdc42 in parallel with an effector, such as p160Rho-kinase, that induces and maintains actin stress fibers in a dominant fashion. Rac1 is not involved in the stellation process per se but appears to induce a dendritogenic effect. Ultimately, it may be stated that Pituicyte stellation is inducible upon mere actin depolymerization, and preventable upon actin organization, be it in the form of stress fibers or in a cortical configuration.
-
A2b receptor mediates adenosine inhibition of taurine efflux from Pituicytes
Biology of the cell, 2007Co-Authors: Patricia M Pierson, Brigitta Peteri-brunbäck, Jean-marc Mienville, D.f. Pisani, M.p. Abbracchio, Lia RossoAbstract:Background information. Recent work suggests that part of the control of vasopressin output is mediated by taurine released from Pituicytes, the astroglial cells of the neurohypophysis. Taurine release, in turn, is stimulated by hypotonic conditions and by vasopressin itself. As adenosine is generated from ATP co-released with vasopressin, it appeared important to study its effects on taurine efflux from Pituicytes. Results. We measured radioactive efflux from cultured Pituicytes and whole neurohypophyses pre-loaded with [3H]taurine. Cultured Pituicytes were also used to study adenosine-receptor mRNA expression. Taurine efflux elicited by hypotonic shocks is ∼30–50% smaller in the presence of 10 μM adenosine or 1 μM NECA (5′-N-ethylcarboxamidoadenosine). Both compounds also inhibited basal efflux in a manner that was not immediately reversible. Agonists of the adenosine A1-, A2a- or A3-receptor subtypes have no relevant effect on basal taurine release, and the A1-receptor antagonist DPCPX (8-cyclopentyl-1,3-dipropylxanthine) has no effect on the inhibition of release by NECA. In turn, the A2b-receptor antagonists MRS 1706 {N-(4-acetylphenyl)-2-[4-(2,3,6,7-tetrahydro-2,6-dioxo-1,3-dipropyl-1H-purin-8-yl)phenoxy]acetamide} or alloxazine partially reverse the inhibition of basal or hypotonicity-evoked efflux by NECA. Both A1- and A2b-receptor mRNAs are expressed in Pituicytes, which is consistent with an A1-receptor-mediated effect on cell morphology and an A2b-receptor-mediated effect on taurine release. Forskolin and dibutyryl cAMP mimic the inhibitory effects of purinergics on basal taurine efflux, and the adenylate cyclase inhibitor DDA (2′,5′-dideoxyadenosine) partially reverses the inhibition of the hypotonic response by NECA. Conclusions. Our results suggest that purinergic inhibition of taurine efflux from Pituicytes operates through A2b receptors coupled to intracellular cAMP increase. They point to a possible modulation of neurohypophysial hormone output by endogenous adenosine released in either physiological or pathological situations.
-
Putative physiological significance of vasopressin V1a receptor activation in rat Pituicytes.
Journal of neuroendocrinology, 2004Co-Authors: Lia Rosso, Brigitta Peteri-brunbäck, Jean-marc MienvilleAbstract:Physiological stimuli operative during, for example, dehydration or lactation, induce neurohypophysial astrocytes (Pituicytes) to undergo reversible morphological changes, which in turn may modulate the release of vasopressin and oxytocin. To study the molecular mechanisms of this morphological plasticity, we used primary cultures of rat Pituicytes. During stimulation with adenosine, Pituicytes become stellate, which is characterized by a round, phase-bright soma and complex arborization, implying major cytoskeletal modifications. Following addition of vasopressin or oxytocin, stellate Pituicytes revert to a flat shape. The effects of both hormones are mediated by V(1a) receptor activation, which also induces biphasic Ca(2+) (i) signals in Pituicytes. Stellation reversal requires Ca(2+)-dependent activation of Cdc42, a small GTPase known to impact on the cytoskeleton. V(1a) receptor activation by vasopressin or oxytocin also stimulates [(3)H]taurine efflux from cultured Pituicytes. As taurine inhibits vasopressin output from neurohypophysial terminals, we postulate a negative-feedback mechanism whereby secreted vasopressin limits its own availability. This stop signal might be reinforced by shape changes elicited by vasopressin in Pituicytes. These results support the concept that, during specific physiological states, Pituicyte V(1a) receptor activation modulates the release of neurohypophysial hormones.
Brigitta Peteri-brunbäck - One of the best experts on this subject based on the ideXlab platform.
-
Status: Postprint (Author’s version)
2016Co-Authors: Lia Rosso, Brigitta Peteri-brunbäck, Valérie Vouret-craviari, Christophe Deroanne, Ellen Van ObberghenAbstract:Vasopressin and oxytocin reverse adenosine-induced Pituicyte stellation via calcium-dependent activation of Cdc4
-
Pituicyte stellation is prevented by RhoA-or Cdc42-dependent actin polymerization.
Cellular and Molecular Neurobiology, 2007Co-Authors: Lia Rosso, Brigitta Peteri-brunbäck, Christophe Deroanne, Ellen Van Obberghen-schilling, Patricia M Pierson, Claire Golfier, Jean-marc MienvilleAbstract:Our aim was to shed light on different steps leading from metabotropic receptor activation to changes in cell shape, such as those that characterize the morphological plasticity of neurohypophysial astrocytes (Pituicytes). Using explant cultures of adult rat Pituicytes, we have previously established that adenosine A1 receptor activation induces stellation via inhibition of RhoA monomeric GTPase and subsequent disruption of actin stress fibers. Here, we rule out RhoA phosphorylation as a mechanism for that inhibition. Rather, our results are more consistent with involvement of a GTPase-activating protein (GAP). siRNA and pull-down experiments suggest that a step downstream of RhoA might involve Cdc42, another GTPase of the Rho family. However, RhoA activation, e.g., in the presence of serum, induces stress fibers, whereas direct Cdc42 activation appears to confine actin within a submembrane - i.e., cortical - network, which also prevents stellation. Therefore, we propose that RhoA may activate Cdc42 in parallel with an effector, such as p160Rho-kinase, that induces and maintains actin stress fibers in a dominant fashion. Rac1 is not involved in the stellation process per se but appears to induce a dendritogenic effect. Ultimately, it may be stated that Pituicyte stellation is inducible upon mere actin depolymerization, and preventable upon actin organization, be it in the form of stress fibers or in a cortical configuration.
-
A2b receptor mediates adenosine inhibition of taurine efflux from Pituicytes
Biology of the cell, 2007Co-Authors: Patricia M Pierson, Brigitta Peteri-brunbäck, Jean-marc Mienville, D.f. Pisani, M.p. Abbracchio, Lia RossoAbstract:Background information. Recent work suggests that part of the control of vasopressin output is mediated by taurine released from Pituicytes, the astroglial cells of the neurohypophysis. Taurine release, in turn, is stimulated by hypotonic conditions and by vasopressin itself. As adenosine is generated from ATP co-released with vasopressin, it appeared important to study its effects on taurine efflux from Pituicytes. Results. We measured radioactive efflux from cultured Pituicytes and whole neurohypophyses pre-loaded with [3H]taurine. Cultured Pituicytes were also used to study adenosine-receptor mRNA expression. Taurine efflux elicited by hypotonic shocks is ∼30–50% smaller in the presence of 10 μM adenosine or 1 μM NECA (5′-N-ethylcarboxamidoadenosine). Both compounds also inhibited basal efflux in a manner that was not immediately reversible. Agonists of the adenosine A1-, A2a- or A3-receptor subtypes have no relevant effect on basal taurine release, and the A1-receptor antagonist DPCPX (8-cyclopentyl-1,3-dipropylxanthine) has no effect on the inhibition of release by NECA. In turn, the A2b-receptor antagonists MRS 1706 {N-(4-acetylphenyl)-2-[4-(2,3,6,7-tetrahydro-2,6-dioxo-1,3-dipropyl-1H-purin-8-yl)phenoxy]acetamide} or alloxazine partially reverse the inhibition of basal or hypotonicity-evoked efflux by NECA. Both A1- and A2b-receptor mRNAs are expressed in Pituicytes, which is consistent with an A1-receptor-mediated effect on cell morphology and an A2b-receptor-mediated effect on taurine release. Forskolin and dibutyryl cAMP mimic the inhibitory effects of purinergics on basal taurine efflux, and the adenylate cyclase inhibitor DDA (2′,5′-dideoxyadenosine) partially reverses the inhibition of the hypotonic response by NECA. Conclusions. Our results suggest that purinergic inhibition of taurine efflux from Pituicytes operates through A2b receptors coupled to intracellular cAMP increase. They point to a possible modulation of neurohypophysial hormone output by endogenous adenosine released in either physiological or pathological situations.
-
Putative physiological significance of vasopressin V1a receptor activation in rat Pituicytes.
Journal of neuroendocrinology, 2004Co-Authors: Lia Rosso, Brigitta Peteri-brunbäck, Jean-marc MienvilleAbstract:Physiological stimuli operative during, for example, dehydration or lactation, induce neurohypophysial astrocytes (Pituicytes) to undergo reversible morphological changes, which in turn may modulate the release of vasopressin and oxytocin. To study the molecular mechanisms of this morphological plasticity, we used primary cultures of rat Pituicytes. During stimulation with adenosine, Pituicytes become stellate, which is characterized by a round, phase-bright soma and complex arborization, implying major cytoskeletal modifications. Following addition of vasopressin or oxytocin, stellate Pituicytes revert to a flat shape. The effects of both hormones are mediated by V(1a) receptor activation, which also induces biphasic Ca(2+) (i) signals in Pituicytes. Stellation reversal requires Ca(2+)-dependent activation of Cdc42, a small GTPase known to impact on the cytoskeleton. V(1a) receptor activation by vasopressin or oxytocin also stimulates [(3)H]taurine efflux from cultured Pituicytes. As taurine inhibits vasopressin output from neurohypophysial terminals, we postulate a negative-feedback mechanism whereby secreted vasopressin limits its own availability. This stop signal might be reinforced by shape changes elicited by vasopressin in Pituicytes. These results support the concept that, during specific physiological states, Pituicyte V(1a) receptor activation modulates the release of neurohypophysial hormones.
-
Vasopressin and oxytocin reverse adenosine-induced Pituicyte stellation via calcium-dependent activation of Cdc42.
The European journal of neuroscience, 2002Co-Authors: Lia Rosso, Brigitta Peteri-brunbäck, Valérie Vouret-craviari, Christophe Deroanne, Ellen Van Obberghen-schilling, Jean-marc MienvilleAbstract:In view of the potential impact of Pituicyte morphology on neurohypophysial hormone secretion, we have studied the mechanisms involved in the shape changes induced by vasopressin (AVP) and oxytocin (OXT) in cultured rat Pituicytes. Pituicytes induced to become stellate in the presence of 10 mM adenosine revert to their nonstellate shape ~20 min after application of AVP or OXT. The IC50 for this effect is 0.1 nM for AVP and 36 nM for OXT. Both agonists induce Ca 2+ signals in Pituicytes, comprised of a transient peak and a plateau phase that is dependent on the presence of extracellular Ca 2+ . The EC50 values of AVP for the transient and sustained responses are 4.5 and 0.1 nM, respectively; corresponding values for OXT are 180 and 107 nM .W e determined pharmacologically that these hormone-induced Ca 2+ signals are mediated by the V1a subtype of vasopressin receptors, similar to what we previously observed for hormone-induced reversal of stellation. Removal of extracellular Ca 2+ or chelation of intracellular Ca 2+ partially prevented AVP from reversing stellation, suggesting a role for Ca 2+ in this event. We previously established that adenosine-induced stellation of Pituicytes occurs via RhoA inhibition. However, pharmacological experiments and pull-down assays presented here show that AVP-induced reversal of stellation does not involve RhoA activation. Rather, AVP was found to induce a time-dependent activation of Cdc42, another small GTPase involved in cytoskeletal plasticity. Activation of Cdc42 by AVP is sensitive to intra- and extracellular Ca 2+ depletion, similar to AVP-induced reversal of stellation. Furthermore, AVP-induced reversal of stellation is blocked by expression of an NWASP fragment known to inhibit endogenous Cdc42.
R.j. Bicknell - One of the best experts on this subject based on the ideXlab platform.
-
Dynorphin 1-17 delays the vasopressin induced mobilization of intracellular calcium in cultured astrocytes from the rat neural lobe.
Journal of neuroendocrinology, 1993Co-Authors: C. J. C. Boersma, W T Mason, F.w. Van Leeuwen, W. G. O'brien, G. J. Law, R.j. BicknellAbstract:Opioid peptides are present in nerve terminals in the rat neural lobe where they partially coexist with vasopressin. Morphological findings suggest that these neuropeptides are released onto Pituicytes, which is in agreement with a possible role for the Pituicyte in oxytocin and vasopressin release from the neural lobe. Pituicytes in culture respond to vasopressin with a mobilization of calcium from intracellular stores. In the present study this vasopressin induced increase in intracellular free calcium levels was both delayed and decreased by pre-exposure to dynorphin 1–17, while dynorphin 1–17 by itself did not affect basal calcium levels. All effects of dynorphin 1–17 could be blocked with naloxone. The present results suggest that opioid receptors are present on Pituicytes and are coupled to a second messenger pathway by which opioid peptides may inhibit inositol phosphate dependent calcium mobilization by other neuropeptides, such as vasopressin.
-
arginine vasopressin mobilises intracellular calcium via v1 receptor activation in astrocytes Pituicytes cultured from adult rat neural lobes
Brain Research, 1992Co-Authors: Glenn I. Hatton, R.j. Bicknell, J Hoyland, R Bunting, W T MasonAbstract:Abstract An extremely close association exists between the membranes of the neurosecretory endings and the resident astrocytes (Pituicytes) of the neurohypophysis. Indeed, synaptoid contacts involving neurosecretory vesicle-containing axons contacting Pituicytes have been observed. suggesting Pituicytes as targets of the products released from neurosecretory axons. We have investigated the effects of various neural lobe peptides on Pituicytes in primary culture from adult neurohypophyses. Using Fura-2 loaded cells and dynamic ratio imaging, we have determined that arginine vasopressin (AVP) or V1- but not V2-receptor agonists, mobilise potuicyte intracellular Ca2+([Ca2+]i) in the absence of extracellular Ca2+. AVP was consistently effective at concentrations of 10 nM or higher in elevating [Ca2+]i by 200–1000 nM. These responses could be blocked by V1-antagonists and were shown to be associated with accumulation of phosphoinositides. Oxytocin was also found to mobilise [ [Ca2+]i but was effective only at higher concentrations than for AVP. Oxytocin-evoked [Ca2+]i elevations were also blocked by V1-antagonists. Raising [K+]0 was ineffective in changing [Ca2+]i suggesting that these cells lack voltage-gated Ca2+ channels. We conclude that Pituicytes possess V1-receptors, activation of which mobilises [Ca2+]i, possibly functioning to initiate a Ca2+-activated K+ conductance which could contribute to further depolarisation of secretory terminals and facilitate exocytosis.
-
Adrenalin activation of beta 2-adrenoceptors stimulates morphological changes in astrocytes (Pituicytes) cultured from adult rat neurohypophyses.
Brain research bulletin, 1991Co-Authors: Glenn I. Hatton, Simon M. Luckman, R.j. BicknellAbstract:Neurohypophysial astrocytes, the Pituicytes, are known to undergo morphological changes in vivo in response to stimuli that increase the demand for hormone secretion. Similar changes have been induced by beta-adrenergic stimulation both in the isolated, but otherwise intact, neural lobe and in Pituicytes cultured from adult rats. Since the predominant beta-receptor subtype in the neural lobe is beta 2, we investigated the possibility that beta 2-receptor activation is mainly responsible for the observed Pituicyte responses. In one experiment, cultured Pituicytes were induced by noradrenalin to change from flattened amorphous to stellate morphology. Addition of the beta 2-antagonist IPS 339, but not the beta 1-antagonist practolol, significantly reduced (by 30-60%) the number of cells transformed by noradrenalin. In a second experiment, adrenalin, by definition a more potent beta 2-agonist, transformed significantly more Pituicytes into stellate shapes than did noradrenalin at the same concentrations (100% vs. 60% increase, respectively). These results support the idea that beta 2-adrenergic receptors are involved in neurohypophysial plasticity. Also, since the neural lobe is outside of the bloodbrain barrier, these findings suggest that adrenal catecholamines participate in altering Pituicyte morphology.
Christophe Deroanne - One of the best experts on this subject based on the ideXlab platform.
-
Status: Postprint (Author’s version)
2016Co-Authors: Lia Rosso, Brigitta Peteri-brunbäck, Valérie Vouret-craviari, Christophe Deroanne, Ellen Van ObberghenAbstract:Vasopressin and oxytocin reverse adenosine-induced Pituicyte stellation via calcium-dependent activation of Cdc4
-
Pituicyte stellation is prevented by RhoA-or Cdc42-dependent actin polymerization.
Cellular and Molecular Neurobiology, 2007Co-Authors: Lia Rosso, Brigitta Peteri-brunbäck, Christophe Deroanne, Ellen Van Obberghen-schilling, Patricia M Pierson, Claire Golfier, Jean-marc MienvilleAbstract:Our aim was to shed light on different steps leading from metabotropic receptor activation to changes in cell shape, such as those that characterize the morphological plasticity of neurohypophysial astrocytes (Pituicytes). Using explant cultures of adult rat Pituicytes, we have previously established that adenosine A1 receptor activation induces stellation via inhibition of RhoA monomeric GTPase and subsequent disruption of actin stress fibers. Here, we rule out RhoA phosphorylation as a mechanism for that inhibition. Rather, our results are more consistent with involvement of a GTPase-activating protein (GAP). siRNA and pull-down experiments suggest that a step downstream of RhoA might involve Cdc42, another GTPase of the Rho family. However, RhoA activation, e.g., in the presence of serum, induces stress fibers, whereas direct Cdc42 activation appears to confine actin within a submembrane - i.e., cortical - network, which also prevents stellation. Therefore, we propose that RhoA may activate Cdc42 in parallel with an effector, such as p160Rho-kinase, that induces and maintains actin stress fibers in a dominant fashion. Rac1 is not involved in the stellation process per se but appears to induce a dendritogenic effect. Ultimately, it may be stated that Pituicyte stellation is inducible upon mere actin depolymerization, and preventable upon actin organization, be it in the form of stress fibers or in a cortical configuration.
-
Vasopressin and oxytocin reverse adenosine-induced Pituicyte stellation via calcium-dependent activation of Cdc42.
The European journal of neuroscience, 2002Co-Authors: Lia Rosso, Brigitta Peteri-brunbäck, Valérie Vouret-craviari, Christophe Deroanne, Ellen Van Obberghen-schilling, Jean-marc MienvilleAbstract:In view of the potential impact of Pituicyte morphology on neurohypophysial hormone secretion, we have studied the mechanisms involved in the shape changes induced by vasopressin (AVP) and oxytocin (OXT) in cultured rat Pituicytes. Pituicytes induced to become stellate in the presence of 10 mM adenosine revert to their nonstellate shape ~20 min after application of AVP or OXT. The IC50 for this effect is 0.1 nM for AVP and 36 nM for OXT. Both agonists induce Ca 2+ signals in Pituicytes, comprised of a transient peak and a plateau phase that is dependent on the presence of extracellular Ca 2+ . The EC50 values of AVP for the transient and sustained responses are 4.5 and 0.1 nM, respectively; corresponding values for OXT are 180 and 107 nM .W e determined pharmacologically that these hormone-induced Ca 2+ signals are mediated by the V1a subtype of vasopressin receptors, similar to what we previously observed for hormone-induced reversal of stellation. Removal of extracellular Ca 2+ or chelation of intracellular Ca 2+ partially prevented AVP from reversing stellation, suggesting a role for Ca 2+ in this event. We previously established that adenosine-induced stellation of Pituicytes occurs via RhoA inhibition. However, pharmacological experiments and pull-down assays presented here show that AVP-induced reversal of stellation does not involve RhoA activation. Rather, AVP was found to induce a time-dependent activation of Cdc42, another small GTPase involved in cytoskeletal plasticity. Activation of Cdc42 by AVP is sensitive to intra- and extracellular Ca 2+ depletion, similar to AVP-induced reversal of stellation. Furthermore, AVP-induced reversal of stellation is blocked by expression of an NWASP fragment known to inhibit endogenous Cdc42.
-
RhoA inhibition is a key step in Pituicyte stellation induced by A(1)-type adenosine receptor activation.
Glia, 2002Co-Authors: Lia Rosso, Brigitta Peteri-brunbäck, Valérie Vouret-craviari, Christophe Deroanne, Jean-denis Troadec, Sylvie Thirion, Ellen Van Obberghen-schilling, Jean-marc MienvilleAbstract:Pituicyte stellation in vitro represents a useful model with which to study morphological changes that occur in vivo in these cells during times of high neurohypophysial hormone output. This model has helped us establish the hypothesis of a purinergic regulation of Pituicyte morphological plasticity. We first show that ATP induces stellation in 37% of Pituicytes, an effect that is secondary to the metabolism of ATP to adenosine. Adenosine-induced stellation of Pituicytes appears to be mediated by A(1)-type receptors. The effect is independent of intracellular calcium and does not involve the mitogen-activated protein kinase pathway. The basal (nonstellate) state of Pituicytes depends on tonic activation of a Rho GTPase because both C3 transferase (a Rho inhibitor) and Y-27632 (an inhibitor of p160Rho kinase) can induce stellation. Lysophosphatidic acid, a Rho activator, blocks the morphogenic effect of adenosine dose-dependently. Using a specific RhoA pull-down assay, we also show that downregulation of activated RhoA is the key event coupling A(1) receptor activation to Pituicyte stellation, via F-actin depolymerization and microtubule reorganization. Finally, both vasopressin and oxytocin can prevent or reverse adenosine-induced stellation. The effects of vasopressin, and those of high concentrations of oxytocin, are mediated through V(1a) receptors. Placed within the context of the relevant literature, our data suggest the possibility of a purinergic regulation of Pituicyte morphological plasticity and subsequent modulation of hormone release, with these hormones providing a negative feedback mechanism.