Dexamethasone Does Not Prevent Seven-Day ADX-Induced Apoptosis in the Dentate Gyrus of the Rat Hippocampus

Long-term adrenalectomy (ADX) is known to result in apoptosis within the dentate gyrus of the rat hippocampus. While the underlying mechanism is still unclear, adrenal steroids appear to play a pivotal role in granule cell survival, as administration of the mineralocorticoid receptor (MR) agonists, corticosterone and aldosterone, to ADX rats results in protection against the ADX-induced effect. The consequence of administration of the glucocorticoid receptor (GR) agonists, dexamethasone and RU28362, however, is less clear, and either complete or only partial protection for the ADX animal has been reported. This study investigated further the role played by GR in the degenerative process. After establishing the characteristics of seven-day ADX-induced apoptosis in the young male Wistar rat, the effect of chronically-implanted, subcutaneous pellets containing various doses of dexamethasone and corticosterone, on ADX-induced apoptosis was studied. Both high and low doses of corticosterone were found to be protective. In contrast to some other studies, however, neither dose of dexamethasone had any obvious protective effect and rather seemed to increase apoptosis in dentate gyrus of intact animals. Intracerebroventricular infusion of dexamethasone for seven days was also found to be ineffective in preventing apoptosis, demonstrating that it is occupation of MR, rather than GR, which is crucial to dentate gyrus granule cell survival.     

Why Dexamethasone Poorly Penetrates in Brain

Dexamethasone poorly penetrates in brain. A tracer amount of [3H]-dexamethasone administered to adrenalectomized rats or mice is poorly retained by glucocorticoid receptors in brain, while pituitary corticotrophs containing equivalent amounts of these receptors accumulate and retain large amounts of this synthetic steroid. However, adrenalectomized mice with a genetic disruption of the multiple drug resistance (mrd1a) gene have a tenfold increase of [3H]-dexamethasone uptake in brain glucocorticoid target sites reaching levels observed in the pituitary. These data demonstrate that dexamethasone is extruded from brain by the mrd1a-encoded P-glycoproteins. The data support the concept of a pituitary site of action of dexamethasone in blockade of stress-induced ACTH release, which implies that chronic dexamethasone treatment does not replace the endogenous corticosteroids depleted from brain mineralocorticoid (MRs) and glucocorticoid receptors (GRs). Dexamethasone, therefore, causes a profound disturbance in the balance of these two receptor types in hippocampus, which is an unfavourable condition threatening the neuronal integrity of this brain structure through the expression of noxious genes.     

Discovering New Ways of Moving: Observational Analysis of Motor Creativity While Dancing Contact Improvisation and the Influence of the Partner

Contact improvisation (CI) is a form of dance based on motor creativity, improvisation and the physical contact between different improvisers dancing together. This will generate different ways of moving and a varied use of motor creativity depending on the dancers involved. This study aims to observe the differences in movement generation depending on the partner by using OSMOS (Observational System of Motor Skills; Castañer & Camerino 2006; Castañer et al., 2009). Four contact improvisers were video‐recorded while dancing in duets. Data were analysed by three observers using Theme Coder software (Magnusson, 1996) for the detection of T‐patterns and the production of event frequency charts. The results show that (1) the motor skills that appear most frequently are the conduction of partners, elevations, spatial level changes and turns; (2) motor creativity is affected by the partner, as there is a reciprocal influence in the dance; and (3) motor creativity is enhanced by interaction with a partner.