ABSTRACT
The 2012 London Olympic and Paralympic Games were widely regarded as an organisational and sporting success for the United Kingdom. Therefore, it is prudent to consider what other large, public endeavours might learn from the Games' success. Team GB worked to develop a positive team culture based around shared values. This is something the National Health Service (NHS) could learn from, as an organisation which can appear to lack this culture. The NHS should also work harder to adopt evidence-based practices, and to adopt them quickly, as is often the case in sport. Sport is the ultimate example of transparent results reporting, and the NHS ought to consider systematic reporting of risk-adjusted performance data, which may drive improved performance. The NHS should pay attention to the experiences of successful Olympic sports with centralised centres of excellence, and to medical data which suggests that better outcomes result from centres of excellence. The NHS and wider government should look to Olympic athletes and place more emphasis on prevention of disease by encouraging positive lifestyle choices. Finally, the NHS should develop private sector partnerships carefully. We must look to gather knowledge and ideas from every area of life in pursuit of excellence in the NHS. Experience of the Olympics offers a number of instructive lessons.
ABSTRACT
The formation of new neurons continues into adult life in the dentate gyrus of the rat hippocampus, as in many other species. Neurogenesis itself turns out to be highly labile, and is regulated by a number of factors. One of these is the serotoninergic system: treatment with drugs (such as the SSRI fluoxetine) markedly stimulates mitosis in the progenitor cells of the dentate gyrus. But this process has one remarkable feature: it takes at least 14 days of continuous treatment to be effective. This is despite the fact that the pharmacological action of fluoxetine occurs within an hour or so of first administration. This paper explores the role of BDNF in this process, using the effect of a Trk antagonist (K252a) on the labelling of progenitor cells with the mitosis marker Ki67 and the associated expression of pCREB and Wnt3a. These experiments show that (i) Fluoxetine increased Ki67 counts, as well as pCREB and Wnt3a expression in the dentate gyrus. The action of fluoxetine on the progenitor cells and on pCREB (but not Wnt3a) depends upon Trk receptor activation, since it was prevented by icv infusion of K252a. (ii) These receptors are required for both the first 7 days of fluoxetine action, during which no apparent change in progenitor mitosis occurs, as well as the second 7 days. Increased pCREB was always associated with progenitor cell mitosis, but Wnt3a expression may be necessary but not sufficient for increased progenitor cell proliferation. These results shed new light on the action of fluoxetine on neurogenesis in the adult dentate gyrus, and have both clinical and experimental interest.
