cAMP Stimulation of Vasopressin and Oxytocin Release and Regulation of Vasopressin mRNA Stability: Role of Auto-Facilitation

2001 ◽  
Vol 13 (2) ◽  
pp. 158-165
Author(s):  
Z. Song ◽  
H. E. Sidorowicz ◽  
C. D. Sladek
Keyword(s):  
Mrna Stability ◽  
Oxytocin Release ◽  
Camp Stimulation ◽  
Stimulation Of

scholarly journals cAMP induces a rapid and reversible modification of the chemotactic receptor in Dictyostelium discoideum.

1985 ◽  
Vol 100 (3) ◽  
pp. 715-720 ◽  
Author(s):  
C Klein ◽  
J Lubs-Haukeness ◽  
S Simons
Keyword(s):  
Dictyostelium Discoideum ◽  
Concentration Dependence ◽  
Time Course ◽  
Camp Synthesis ◽  
Sds Page ◽  
Reversible Modification ◽  
Camp Receptor ◽  
Camp Stimulation ◽  
Stimulation Of

Stimulation, within 1 min after cAMP stimulation, of aggregation-competent Dictyostelium discoideum amebae was found to cause a rapid (within 1 min) modification of the cell's surface cAMP receptor. The modified receptor migrated on SDS PAGE as a 47,000-mol-wt protein, as opposed to a 45,000-mol-wt protein labeled on unstimulated cells. The length of time this modified receptor could be detected depended upon the strength of the cAMP stimulus: 3-4 min after treatment with 10(-7) M cAMP, cells no longer possessed the 47,000-mol-wt form of the cAMP receptor. Instead, the 45,000-mol-wt form was present. Stimulation of cells with 10(-5) M cAMP, however, resulted in the persistent (over 15 min) expression of the modified receptor. The time course, concentration dependence, and specificity of stimulus for this cAMP-induced shift in the cAMP receptor were found to parallel the cAMP-stimulated phosphorylation of a 47,000-mol-wt protein. In addition, both phenomena were shown to occur in the absence of endogenous cAMP synthesis. The possibility that the cAMP receptor is phosphorylated in response to cAMP stimulation, and the role of this event in cell desensitization, are discussed.

scholarly journals Noradrenergic control of central oxytocin release during lactation in rats

1998 ◽  
Vol 274 (3) ◽  
pp. E453-E458 ◽  
Author(s):  
Steven L. Bealer ◽  
William R. Crowley
Keyword(s):  
Cerebrospinal Fluid ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Additional Experiment ◽  
Adrenergic Agonist ◽  
Magnocellular Nuclei ◽  
Artificial Cerebrospinal Fluid ◽  
Oxytocin Release ◽  
Stimulation Of

Noradrenergic systems regulate the systemic release of oxytocin (OT) in lactating rats. However, a role for norepinephrine (NE) in release of OT within the magnocellular nuclei during suckling has not been established. These studies were designed to determine 1) if suckling induces NE release in the supraoptic (SON) and paraventricular (PVN) nuclei of conscious rats and 2) the role of NE in the central, intranuclear release of OT within these nuclei. Female Holtzman rats were implanted with microdialysis probes adjacent to the PVN or SON on lactation days 8- 12. The following day, the pups were isolated from the dams for 4 h. Microdialysis probes were perfused with artificial cerebrospinal fluid (ACSF) or with ACSF containing an α- or a β-adrenergic receptor antagonist. Dialysate was collected before, during, and after suckling and analyzed for NE or OT. In an additional experiment, an α- or β-adrenergic agonist was administered via the microdialysis probes into the PVN in nonsuckled, lactating rats. Extracellular NE increased in the PVN during suckling but was not detectable in the SON. OT concentrations in dialysates from the PVN and SON significantly increased during suckling. Blockade of either α- (in both PVN and SON) or β- (PVN) adrenergic receptors prevented the suckling-induced increase in central OT release. OT release was increased in nonsuckled, lactating rats by central application of either an α- or β-adrenergic agonist. These data demonstrate that intranuclear NE release is increased in the PVN by suckling and that subsequent stimulation of both α- and β-noradrenergic receptors mediates intranuclear OT release.

Involvement of the Tis11b/Berg36 Family in the Regulation of B-CLL Surivival and Differentiation.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4936-4936
Author(s):  
Maria Baou ◽  
John Murphy ◽  
Kwee L. Yong ◽  
Robert Carr ◽  
Andrew P. Jewell
Keyword(s):  
Cell Cycle ◽  
Gene Regulation ◽  
Mrna Stability ◽  
Statistical Significance ◽  
Spontaneous Apoptosis ◽  
Basal Expression ◽  
Transcriptional Gene Regulation ◽  
Regulation Of Cell Cycle ◽  
Stimulation Of

Abstract Tis11b/Berg36 is a member of a family of proteins involved in post-transcriptional gene regulation. Members of this family bind to AU rich elements in certain mRNA species and increase mRNA stability. mRNA that contain AU rich elements and can be regulated in this way include molecules involved in the regulation of apoptosis eg bcl-2 and several cytokines eg TNF, IL-2. We have recently shown that Tis11b/Berg36 is involved in the regulation of apoptosis following Rituximab treatment of CLL cells suggesting a pro-apoptotic role of this gene in CLL cells. Thus B-CLL were stimulated with IL-4, anti-CD40, anti-CD40+IL-4 and PMA. It was found that IL-4, CD40 and their combination significantly inhibited spontaneous apoptosis while PMA was able to inhibit spontaneous apoptosis in some but not all patients tested and the overall effect did not reached statistical significance. Unexpectedly Tis11b/Berg36 mRNA remained unchanged following IL-4 treatment, but expression was induced following anti-CD40 or PMA treatment. Because it was found that regulation of Tis11b/Berg36 mRNA following the latter two treatments was under the control of NF-κB pathway and not p38 (as found for Rituximab treatment) it was hypothesized that this gene may be involved in the regulation of cell cycle or differentiation of B-CLL cells. Indeed it was found that stimulation of B-CLL cells with either PMA or anti-CD40 resulted in increase in sIgM as a marker of B-CLL differentiation. CLL cells were also found to express high basal levels of two other members of this family, Tis11 and Tis11d. From these stimuli, IL-4 or anti-CD40 were found to downregulate the basal expression of Tis11 mRNA. These data suggest that members of the Tis11b/Berg36 family are involved in the regulation of apoptosis and differentiation in B-CLL cells.

scholarly journals Multiple α1-adrenergic receptor subtypes support synergistic stimulation of vasopressin and oxytocin release by ATP and phenylephrine

2010 ◽  
Vol 299 (6) ◽  
pp. R1529-R1537 ◽  
Author(s):  
Zhilin Song ◽  
Dayane A. Gomes ◽  
Wanida Stevens ◽  
Celia D. Sladek
Keyword(s):  
Adrenergic Receptor ◽  
Supraoptic Nucleus ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Simultaneous Exposure ◽  
Oxytocin Release ◽  
Subtype Selective ◽  
Stimulation Of ◽  
Sustained Activation

Simultaneous exposure of explants of the hypothalamo-neurohypophyseal system (HNS) to ATP and the α1-adrenergic receptor (α1-R) agonist, phenylephrine (ATP+PE) induces a synergistic stimulation of vasopressin and oxytocin (VP/OT) release that is sustained for hours ( 23 ). The current studies confirm that the synergism is dependent upon activation of α1-R by demonstrating that an α1-R antagonist prevents the response. The role of the α1A, B, and D-adrenergic receptor subtypes in the synergistic effect of ATP+PE on intracellular calcium ([Ca2+]i) in supraoptic nucleus (SON) neurons and VP/OT release from neural lobe was evaluated. The increase in [Ca2+]i induced by PE in SON predominantly reflects release from intracellular stores and is mediated by activation of the α1A adrenergic receptor subtype. The α1A subtype is also required for the sustained elevation in [Ca2+]i induced by ATP+PE. In contrast, although synergistic stimulation of VP/OT release was eliminated by removal of PE and was blunted by benoxathian, an α1-R antagonist that is not subtype selective, no single α1-R subtype selective antagonist prevented sustained stimulation of VP/OT release by ATP+PE. Thus, sustained activation of α1-R is essential for the synergistic VP and OT response to ATP+PE, but multiple α1-R subtypes can support the response. Redundancy amongst the α1-R subunits in supporting this response is consistent with the predicted importance of the response for sustaining the elevated VP release required to prevent cardiovascular collapse during hemorrhage and sepsis.

Stimulation of Ca(2+)-dependent exocytosis of the sperm acrosome by cAMP acting downstream of phospholipase A2

Reproduction ◽  
2000 ◽  
pp. 57-68 ◽  
Author(s):  
J Garde ◽  
ER Roldan
Keyword(s):  
Arachidonic Acid ◽  
Phospholipase A2 ◽  
Phospholipase C ◽  
Phosphodiesterase Inhibitors ◽  
Dibutyryl Camp ◽  
Camp Phosphodiesterase ◽  
Ram Sperm ◽  
Camp Formation ◽  
Stimulation Of

Spermatozoa undergo exocytosis in response to agonists that induce Ca2+ influx and, in turn, activation of phosphoinositidase C, phospholipase C, phospholipase A2, and cAMP formation. Since the role of cAMP downstream of Ca2+ influx is unknown, this study investigated whether cAMP modulates phospholipase C or phospholipase A2 using a ram sperm model stimulated with A23187 and Ca2+. Exposure to dibutyryl-cAMP, phosphodiesterase inhibitors or forskolin resulted in enhancement of exocytosis. However, the effect was not due to stimulation of phospholipase C or phospholipase A2: in spermatozoa prelabelled with [3H]palmitic acid or [14C]arachidonic acid, these reagents did not enhance [3H]diacylglycerol formation or [14C]arachidonic acid release. Spermatozoa were treated with the phospholipase A2 inhibitor aristolochic acid, and dibutyryl-cAMP to test whether cAMP acts downstream of phospholipase A2. Under these conditions, exocytosis did not occur in response to A23187 and Ca2+. However, inclusion of dibutyryl-cAMP and the phospholipase A2 metabolite lysophosphatidylcholine did result in exocytosis (at an extent similar to that seen when cells were treated with A23187/Ca2+ and without the inhibitor). Inclusion of lysophosphatidylcholine alone, without dibutyryl-cAMP, enhanced exocytosis to a lesser extent, demonstrating that cAMP requires a phospholipase A2 metabolite to stimulate the final stages of exocytosis. These results indicate that cAMP may act downstream of phospholipase A2, exerting a regulatory role in the exocytosis triggered by physiological agonists.

scholarly journals Pre-motor versus motor cerebral cortex neuromodulation for chronic neuropathic pain

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Igor Lavrov ◽  
Timur Latypov ◽  
Elvira Mukhametova ◽  
Brian Lundstrom ◽  
Paola Sandroni ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Cerebral Cortex ◽  
Motor Cortex ◽  
Initial Assessment ◽  
Motor Cortex Stimulation ◽  
Chronic Neuropathic Pain ◽  
Long Term Effect ◽  
Stimulation Of

AbstractElectrical stimulation of the cerebral cortex (ESCC) has been used to treat intractable neuropathic pain for nearly two decades, however, no standardized approach for this technique has been developed. In order to optimize targeting and validate the effect of ESCC before placing the permanent grid, we introduced initial assessment with trial stimulation, using a temporary grid of subdural electrodes. In this retrospective study we evaluate the role of electrode location on cerebral cortex in control of neuropathic pain and the role of trial stimulation in target-optimization for ESCC. Location of the temporary grid electrodes and location of permanent electrodes were evaluated in correlation with the long-term efficacy of ESCC. The results of this study demonstrate that the long-term effect of subdural pre-motor cortex stimulation is at least the same or higher compare to effect of subdural motor or combined pre-motor and motor cortex stimulation. These results also demonstrate that the initial trial stimulation helps to optimize permanent electrode positions in relation to the optimal functional target that is critical in cases when brain shift is expected. Proposed methodology and novel results open a new direction for development of neuromodulation techniques to control chronic neuropathic pain.

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