Utilizing this treatment it was even possible to recover the normal ocular dominance and to restore visual acuity to adult animals which had grown up with one long-term deprived eye (Pizzorusso et al., 2006). These experiments strongly suggest that one

important function of the adult ECM is to terminate juvenile plasticity and to fix acquired experience-dependent wiring for the adult life. A more recent study by Gogolla et al. (2009) suggests that similar mechanisms may make particular memories, such as fear memories, erasure-resistant, i.e., insensitive to extinction. In young rats, conditioned fear memories can be erased permanently whereas rats older than 3–4 weeks are resistant to this fear extinction. Fear extinction in both adult and young rats selleck products is amygdala-dependent. In this brain structure, PNNs develop between postnatal days 16 and 21. After this critical period fear memory can be reduced by repeated exposure to the conditioned stimulus in the absence of the aversive fear-provoking stimulus. However, in contrast to young animals, fear response is reinstated when the aversive stimulus is presented

again. Similar to the experiments in the visual cortex, removal of the hyaluronan–CSPG-based ECM achieved a rapid and permanent erasure of newly acquired fear memories. Extinction did not take place when fear experience took RNA Synthesis inhibitor place before the application of chondroitinase, suggesting that CSPGs are essential for protecting fear memories from erasure during the acquisition phase (Gogolla et al., 2009; Pizzorusso, 2009). The mechanisms by which the hyaluronan–CSPG-based ECM performs its functions in establishing adult CNS plasticity are still largely unknown. Selleckchem Verteporfin However, a number of studies suggest that the adult ECM is importantly involved in various aspects of synaptic plasticity, which may contribute to the observed phenomena. These aspects include mechanisms of classical (Hebbian) plasticity as well as homeostatic synaptic plasticity and metaplasticity

(see Dityatev & Schachner, 2003; Dityatev & Fellin, 2008 for a comprehensive review). In essence, most functions of the ECM have been reviewed on numerous occasions (for an overview see Table 1). Therefore, for the purpose of this article we will focus in the following sections on few aspects of adult ECM functions that may be important for the understanding of the implementation of adult plasticity mechanisms in the CNS. These are the control of extracellular diffusion events and the control of lateral diffusion of plasma membrane proteins. Finally, we will consider mechanisms to locally modulate ECM functions. The interneuronal communication within neuronal networks is dominated by the diffusive transmission of signaling molecules.