scholarly journals Mitotic activity, modulation of DNA processing, and purinergic signalling in the adult rat auditory brainstem following sensory deafferentation

2019 ◽  
Vol 50 (12) ◽  
pp. 3985-4003
Author(s):  
Robert‐Benjamin Illing ◽  
Helena Buschky ◽  
Annamaria Tadic
Keyword(s):  
Mitotic Activity ◽  
Auditory Brainstem ◽  
Purinergic Signalling ◽  
Adult Rat ◽  
Dna Processing

scholarly journals Antenatal Dexamethasone Treatment Induces Sex-dependent Up-regulation of NTPDase1/CD39 and Ecto-5ʹ-nucleotidase/CD73 in the Rat Fetal Brain

2021 ◽  
Author(s):  
Milica Manojlovic-Stojanoski ◽  
Irena Lavrnja ◽  
Ivana Stevanovic ◽  
Svetlana Trifunovic ◽  
Natasa Ristic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Adverse Effects ◽  
Fetal Brain ◽  
Wistar Rat ◽  
Purinergic Signalling ◽  
Adult Rat ◽  
Cell Adhesion And Migration ◽  
And Migration ◽  
Cd73 Expression ◽  
The Brain

Abstract Dexamethasone (DEX) is frequently used to treat women at risk of preterm delivery, but although indispensable for completion of organ maturation in fetus, antenatal DEX treatment may exert adverse sex-dimorphic neurodevelopmental effects. Literature findings implicated oxidative stress in adverse effects of DEX treatment.. Purinergic signalling is involved in neurodevelopment, and controled by ectonucleotidases, among which in the brain are most abundant ectonucleoside triphosphate diphosphohydrolase 1 (NTPDase1/CD39) and ecto-5ʹ-nucleotidase (e5ʹNT/CD73), which jointly dephosphorylate ATP to adenosine. They are also involved in cell adhesion and migration, critical for brain development. Up-regulation of CD39 and CD73 after DEX treatment was reported in adult rat hippocampus. We investigated the effects of maternal DEX treatment on CD39 and CD73 expression and enzymatic activity in the rat fetal brain of both sexes, in the context of oxidative status of the brain tissue. Fetuses were obtained at embryonic day (ED) 21, from Wistar rat dams treated with 0.5 mg DEX/kg/day, at ED 16, 17, and 18, and brains were processed and used for further analysis. Sex-specific increase in CD39 and CD73 expression and in the corresponding enzyme activities was induced in the brain of antenatally DEX-treated fetuses, more prominently in males. The oxidative stress induction after antenatal DEX treatment, was confirmed in both sexes, altghough showing a slight bias in males. Due to involvement of purinergic system in crucial neurodevelopmental processes, future investigations are needed to determine the role of observed changes in the adverse effects of antenatal DEX treatment.

scholarly journals Temporally Sensitive Trophic Responsiveness of the Adrenalectomized Rat Anterior Pituitary to Dexamethasone Challenge: Relationship between Mitotic Activity and Apoptotic Sensitivity

Endocrinology ◽  
2003 ◽  
Vol 144 (1) ◽  
pp. 212-219 ◽  
Author(s):  
L. A. Nolan ◽  
A. Levy
Keyword(s):  
Cell Cycle ◽  
Mitotic Activity ◽  
Cell Population ◽  
Anterior Pituitary ◽  
Apoptotic Cell ◽  
Apoptotic Response ◽  
Adult Rat ◽  
Step Down ◽  
Induced Apoptosis ◽  
Persistent Elevation

Abstract Depending on timing and dose, exogenous glucocorticoids induce a wave of apoptosis in the adult rat anterior pituitary, a response that is enhanced by adrenalectomy. In this study, we show that the size of the glucocorticoid-sensitive apoptotic population progressively increases during the week following surgical adrenalectomy, plateaus for a further week, then spontaneously declines to levels seen in intact animals by 4 wk. Mitotic activity, in contrast, rises rapidly post adrenalectomy but returns to baseline within 2 wk. Increased mitotic activity precedes the increase in the population of cells that undergo glucocorticoid-induced apoptosis and the subsequent decline in mitotic activity precedes the decline in apoptotic sensitivity despite persistent elevation of hypothalamic CRH and pituitary proopiomelanocortin transcripts. If glucocorticoid exposure is delayed until 4 wk post adrenalectomy when the apoptotic response has returned to baseline, glucocorticoid withdrawal, by transiently increasing mitotic activity, again primes the formation of an expanded glucocorticoid-sensitive apoptotic cell population. These data suggest that apoptotic sensitivity is largely confined to cells that have recently entered the cell cycle. This observation is further corroborated by demonstrating an abrupt glucocorticoid-induced step-down in the bromodeoxyuridine-labeling index to basal levels in rats given daily injections of bromodeoxyuridine during the week following adrenalectomy.

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