Effects of gestational and breastfeeding caffeine exposure in adenosine A1 agonist‐induced antinociception of infant rats

2020 ◽  
Vol 80 (8) ◽  
pp. 709-716
Author(s):  
Iraci L. S. Torres ◽  
José A. F. Assumpção ◽  
Andressa Souza ◽  
Carla Oliveira ◽  
Lauren N. S. Adachi ◽  
...  
Keyword(s):  
Infant Rats ◽  
Adenosine A1 ◽  
Caffeine Exposure

Caffeine Delays Light-entrained Activity and Potentiates Circadian Photic Phase-resetting in Mice

2018 ◽  
Vol 33 (5) ◽  
pp. 523-534 ◽  
Author(s):  
Christina L. Ruby ◽  
Natalie M. Verbanes ◽  
Kaitlyn N. Palmer ◽  
Catherine F. Zisk ◽  
David J. Bunion ◽  
...  
Keyword(s):  
Circadian Clock ◽  
Receptor Antagonist ◽  
High Dose ◽  
Phase Resetting ◽  
Circadian Activity ◽  
Self Administration ◽  
A2a Receptor ◽  
Adenosine A1 ◽  
Caffeine Exposure

Caffeine is widely used to reduce sedation and increase alertness. However, long-term caffeine use may disrupt circadian (daily, 24-h) rhythms and thereby negatively affect health. Here, we examined the effect of caffeine on photic regulation of circadian activity rhythms in mice. We found that entrainment to a standard 12-h light, 12-h dark (LD) photocycle was delayed during oral self-administration of caffeine. Both acute, high-dose caffeine and chronic, oral caffeine exposure potentiated photic phase-delays in mice, suggesting a possible mechanism by which entrainment to LD was delayed. The effect of caffeine on photic phase-resetting was mimicked by administration of adenosine A1, but not A2A, receptor antagonist in mice. Our results support the hypothesis that caffeine interferes with the ability of the circadian clock to respond normally to light.

Performance of binocular and monocular infant rats on the visual cliff.

1969 ◽  
Vol 67 (2, Pt.1) ◽  
pp. 177-181 ◽  
Author(s):  
Richard Lore ◽  
Doris Sawatski
Keyword(s):  
Visual Cliff ◽  
Infant Rats

Adenosine A1 Receptor Antagonist Up-regulates Casp3 and Stimulates Apoptosis Rate in Breast Cancer Cell Line T47D

2020 ◽  
Vol 9 (1) ◽  
pp. 14-20
Author(s):  
Mohammad Zamani Rarani ◽  
Fahimeh Zamani Rarani ◽  
Ali Valiani ◽  
Zeinolabedin Shrifian Dastjerdi ◽  
Elias Kargar Abargouei ◽  
...  
Keyword(s):  
Cell Line ◽  
Cancer Cell Line ◽  
P53 Gene ◽  
T47d Cell ◽  
Adenosine A1 Receptor ◽  
T47d Cells ◽  
Apoptosis Rate ◽  
Adenosine A1 ◽  
T47d Cell Line ◽  
A1 Receptor

Background: Adenosine receptor family, especially A1 type is-overexpressed in breast-derived tumor cells and the P53 gene is mutant in some of these cells while the casps gene is of wild type as well. The aim of this study was to evaluate the effect of the A1 receptor function on cell programmed death or proliferation, as well as the relationship between this receptor stimulation/inhibition and caspase 3 (casp3) expression in T47D cell line that has a mutant and non-functional P53 gene. Materials and Methods: The expression of casps3 was measured by real-time polymerase chain reaction and then flow cytometery and MTT assay were used to assess the apoptotic and proliferation cell rate after the treatment of T47D cells with specific agonist N6-cyclopentyladenosine (CPA) and antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) of this receptor 24, 48, and 72 hours after treatment. Result: Our results indicated that DPCPX significantly induces apoptosis in T47D cells and the rate of survival cell after the reduction of this treatment, especially 72 hours after treatment. Finally, the expression of casp3 was up-regulated by DPCPX treatment, especially in 72 hours while CPA treatment had opposite results (P>0.05). Conclusion: In general, DPCPX could up-regulate casp3 gene expression and subsequently increase the apoptosis rate in T47D cells with casp3 expression without the P53 gene interference. Therefore, adenosine A1 receptor antagonists may be introduced as anti-cancer agents.

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