Many plastic processes employ ectoenzymes that may restore locally ‘juvenile’ environments

in addition to generating new signaling molecules from cell surface and ECM products. The window for this type of research has just been opened and new views on basically important and medically relevant mechanisms of brain plasticity will emerge. These might include a deeper understanding of mental disorders including anxiety disorders (Pizzorusso, 2009), as well as schizophrenia and affective disorders that generally develop after the closure of major critical AP24534 datasheet periods for higher brain functions of the prefrontal cortex after adolescence. We wish to thank Dr Amin Derouiche, Bonn, for providing a photomicrograph for Fig. 1. Research in the authors’ laboratories on this topic is funded by the DFG (GU230/5-1,2,3; HE3604/2-1) and by ERA-Net NEURON (Moddifsyn).

Abbreviations AMPAR AMPA receptor CSPG chondroitin sulfate proteoglycan ECM extracellular matrix ECS extracellular space MMP matrix metalloprotease PNN perineuronal net tPA tissue-type click here plasminogen activator “
“Although it is accepted that new neurons continue to be generated in the hippocampal dentate gyrus (DG) throughout adulthood, it has recently become apparent that this process is not homogeneous, and that a small region of the DG lacks neurogenesis. Here, we show that the relative area of this neurogenesis quiescent zone (NQZ) did not vary

after the peak in hippocampal postnatal neurogenesis and until animals reached adulthood, although the ratio between its actual volume and the total volume of the DG doubled during this time. However, we were able to identify a few mitotic cells that reside within this subregion in early adolescent rats. Furthermore, these cells can be activated, and 1 week of voluntary exercise was enough to significantly increase the number of mitotic cells within the NQZ of adolescent rats. There was, however, no corresponding increase in the number of new neurons in this subregion of the DG, suggesting that some factor necessary to allow these why cells to develop into a mature phenotype is missing. Moreover, the same intervention was ineffective in increasing either proliferation or neurogenesis in older adult rats. Surprisingly, we found no evidence for the existence of an NQZ in the mouse DG, suggesting that the neurogenic process in these two rodent species is differently regulated. Understanding the molecular mechanisms underlying the existence of the NQZ in the rat DG might shed light on the processes that regulate adult neurogenesis and its modulation by factors such as aging and exercise. “
“A selection of influential FEMS publications to celebrate the 40th anniversary of FEMS.