Role of cAMP signalling in winner and loser effects in crayfish agonistic encounters

2016 ◽  
Vol 44 (2) ◽  
pp. 1886-1895 ◽  
Author(s):  
Yuto Momohara ◽  
Hiroki Minami ◽  
Akihiro Kanai ◽  
Toshiki Nagayama
2013 ◽  
Vol 280 (1767) ◽  
pp. 20131514 ◽  
Author(s):  
Mylene M. Mariette ◽  
Charlène Cathaud ◽  
Rémi Chambon ◽  
Clémentine Vignal

Social interactions with adults are often critical for the development of mating behaviours. However, the potential role of other primary social partners such as juvenile counterparts is rarely considered. Most interestingly, it is not known whether interactions with juvenile females improve males’ courtship and whether, similar to the winner and loser effects in a fighting context—outcome of these interactions shapes males’ behaviour in future encounters. We investigated the combined effects of male quality and juvenile social experience on pairing success at adulthood in zebra finches ( Taeniopygia guttata ). We manipulated brood size to alter male quality and then placed males in either same- or mixed-sex juvenile dyads until adulthood. We found that males from reduced broods obtained more copulations and males from mixed-sex dyads had more complete courtships. Furthermore, independent of their quality, males that failed to pair with juvenile females, but not juvenile males, had a lower pairing success at adulthood. Our study shows that negative social experience with peers during adolescence may be a potent determinant of pairing success that can override the effects of early environmental conditions on male attractiveness and thereby supports the occurrence of an analogous process to the loser effect in a mating context.


Behaviour ◽  
1989 ◽  
Vol 109 (1-2) ◽  
pp. 1-19 ◽  
Author(s):  
Lameck M. Phiri ◽  
George F. Turner ◽  
Shaun Cawthraw

AbstractCourtship behaviour was investigated in the sexually monochromatic biparental cichlid, Tilapia mariae, with particular emphasis on the role of submissive behaviour in the process of pair formation. Pair formation successfully occurred when the female had prior residence in the tank, and could occur within a few minutes. Dominant females generally had priority of access to males. In the experiment where pairing occurred, dominant females and males showed practically no overt aggression towards each other. In the confines of a small tank, with no other subordinate conspecifics present, male and female T. mariae did show aggression to one another, but in this case courtship behaviour was entirely absent. Closed-fin postures were employed by both sexes of Tilapia mariae in the early stages of courtship: it is suggested that these served as 'Partner Attack Inhibition' displays. Submissive displays of the kind employed in agonistic encounters are not used in courtship.


2020 ◽  
Vol 12 ◽  
Author(s):  
Leandro Bueno Bergantin

Background: The interactions between Alzheimer´s disease (AD) and major depression can be translated into clinical data showing that depressive patients have had an enhanced risk for developing AD (later in life). The cellular mechanisms involved in these interactions remain under intensive debate in literature. In addition, the role of a Ca2+ homeostasis dysregulation in the pathogenesis of neurodegenerative diseases, like AD, and major depression has been under intensive discussion. Objective: Thus, revealing the interplay between AD and major depression may provide novel insights into the pathogenesis of these diseases. Methods: Publications involving Ca2+ signalling pathways, AD and major depression (alone or combined) were collected by searching multiple databases to find the maximum number of relevant citations (using a search strategy with a high sensitivity for studies of etiology). Results: Ca2+ channel blockers (CCBs), classically prescribed for hypertensive patients, have been demonstrating neuroprotective effects, such as decreasing the incidence of AD in hypertensive patients, including alleviating major depression symptoms. A mechanism under debate is focused on the restoration of the Ca2+ homeostasis. Indeed, previous studies of our own have correlated Ca2+ and cAMP signalling pathways (Ca2+/cAMP signalling) in controlling both the neurotransmitter release and neuronal death. These studies also observed that CCBs can affect Ca2+/cAMP signalling. Conclusion: This review discussed the plausible role of Ca2+/cAMP signalling in the neuroprotective effects of CCBs, including the participation of Ca2+/cAMP signalling in the interactions between major depression and AD. Considering both AD and major depression have become high prevalent medical problems in the world, the comprehension of the interactions between these diseases could improve the drug development.


2001 ◽  
Vol 1 (1) ◽  
pp. 33-45 ◽  
Author(s):  
F ROLLAND ◽  
V WANKE ◽  
L CAUWENBERG ◽  
P MA ◽  
E BOLES ◽  
...  

2014 ◽  
Vol 42 (1) ◽  
pp. 89-97 ◽  
Author(s):  
Owain Llŷr Roberts ◽  
Caroline Dart

The second messenger cAMP plays a central role in mediating vascular smooth muscle relaxation in response to vasoactive transmitters and in strengthening endothelial cell–cell junctions that regulate the movement of solutes, cells and macromolecules between the blood and the surrounding tissue. The vasculature expresses three cAMP effector proteins: PKA (protein kinase A), CNG (cyclic-nucleotide-gated) ion channels, and the most recently discovered Epacs (exchange proteins directly activated by cAMP). Epacs are a family of GEFs (guanine-nucleotide-exchange factors) for the small Ras-related GTPases Rap1 and Rap2, and are being increasingly implicated as important mediators of cAMP signalling, both in their own right and in parallel with the prototypical cAMP target PKA. In the present paper, we review what is currently known about the role of Epac within blood vessels, particularly with regard to the regulation of vascular tone, endothelial barrier function and inflammation.


2020 ◽  
Vol 20 (2) ◽  
pp. 103-109 ◽  
Author(s):  
Leandro B. Bergantin

Background: A correlation between cognitive dysfunctions and brain insulin resistance has been established by several clinical and experimental studies. Consistent data support that people diagnosed with brain insulin resistance, resulted from diabetes, have shown an increased risk of presenting cognitive dysfunctions, clinical signs of dementia and depression, then speculating a role of dysregulations related to insulin signalling in these diseases. Furthermore, it is currently discussed that Ca2+ signalling, and its dysregulations, may be a factor which could correlate with brain insulin resistance and cognitive dysfunctions. Objective: Following this, revealing this interplay between these diseases may provide novel insights into the pathogenesis of such diseases. Methods: Publications covering topics such as Ca2+ signalling, diabetes, depression and dementia (alone or combined) were collected by searching PubMed and EMBASE. Results: The controlling of both neurotransmitters/hormones release and neuronal death could be achieved through modulating Ca2+ and cAMP signalling pathways (Ca2+/cAMP signalling). Conclusion: Taking into account our previous reports on Ca2+/cAMP signalling, and considering a limited discussion in the literature on the role of Ca2+/cAMP signalling in the link between cognitive dysfunctions and brain insulin resistance, this article has comprehensively discussed the role of these signalling pathways in this link (between cognitive dysfunctions and brain insulin resistance).


2020 ◽  
Vol 20 (3) ◽  
pp. 321-327
Author(s):  
Leandro B. Bergantin

Objective: Asthma is correlated with a higher risk of manifesting other diseases, including hypertension, diabetes, obesity, psychiatric and neurological diseases, and cancer. Therefore, revealing this interplay between asthma and these illnesses may provide novel insights into their pathogenesis. Results: It is highly debated that dysregulation of Ca2+ homeostasis is involved in the pathogenesis of these maladies. Not surprisingly, calcium (Ca2+) channel blockers (CCBs), classically used as antihypertensive medicines, have been demonstrating off-label effects such as alleviating asthma symptoms, in addition to antidiabetic, antiobesity, anticancer and antineurodegenerative effects. Our studies about Ca2+/cAMP signalling may shed some new light on this field. Conclusion: Thus, considering that asthma and associated illnesses such as hypertension, diabetes, obesity, cancer and neurodegenerative diseases have become highly prevalent medical problems in the world, the comprehension of this interplay between asthma and other disorders could improve drug therapy.


2003 ◽  
Vol 375 (1) ◽  
pp. 167-174 ◽  
Author(s):  
Florence GOUYON ◽  
Cercina ONESTO ◽  
Veronique DALET ◽  
Gilles PAGES ◽  
Armelle LETURQUE ◽  
...  

In intestinal cells, levels of the fructose transporter GLUT5 are increased by glucose and to a greater extent by fructose. We investigated the mechanism by which fructose increases GLUT5 expression. In Caco-2 cells, fructose and glucose increased activity of the −2500/+41 GLUT5 promoter to the same extent. cAMP also activated the GLUT5 promoter. However, if a protein kinase A inhibitor was used to block cAMP signalling, extensive GLUT5 mRNA degradation was observed, with no change in basal transcription levels demonstrating the involvement of cAMP in GLUT5 mRNA stability. Indeed, the half-life of GLUT5 mRNA was correlated (R2=0.9913) with cellular cAMP levels. Fructose increased cAMP concentration more than glucose, accounting for the stronger effect of fructose when compared with that of glucose on GLUT5 production. We identified several complexes between GLUT5 3′-UTR RNA (where UTR stands for untranslated region) and cytosolic proteins that might participate in mRNA processing. Strong binding of a 140 kDa complex I was observed in sugar-deprived cells, with levels of binding lower in the presence of fructose and glucose by factors of 12 and 6 respectively. This may account for differences in the effects of fructose and glucose. In contrast, the amounts of two complexes of 96 and 48 kDa increased equally after stimulation with either glucose or fructose. Finally, PABP (polyadenylated-binding protein)-interacting protein 2, a destabilizing partner of PABP, was identified as a component of GLUT5 3′-UTR RNA–protein complexes. We conclude that the post-transcriptional regulation of GLUT5 by fructose involves increases in mRNA stability mediated by the cAMP pathway and Paip2 (PABP-interacting protein 2) binding.


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