This result suggests that the loss of inhibitory structures may reflect a general reduction of inhibition after a decrease in cortical activity, which could be a result of either decreased activity levels in the inhibitory neurons themselves or in the activity levels of the network (as in Hartman et al., 2006). Enzalutamide supplier The loss of spines and boutons following complete lesions, however, occurred over a somewhat slower time course than after focal lesions. One possible explanation for these differences in timing is that in the case of focal retinal lesions there is not only an overall drop in activity, but also competition between silenced and
still active inputs stemming from cells located in regions of cortex adjacent to the LPZ. As competitive or Hebbian plasticity Selleck Autophagy inhibitor has been shown to develop in vitro over the time course of
minutes to hours (Kirkwood and Bear, 1995), as opposed to homeostatic plasticity, which results from input loss and occurs over a period of days (Turrigiano and Nelson, 2004), it is conceivable that this competition causes a more rapid removal of silent inputs than the overall reduction of activity levels following complete retinal lesions. We have previously demonstrated that structural changes in excitatory cells associated with functional recovery after a retinal lesion were restricted to the LPZ (Keck et al., 2008). In contrast, the structural changes of inhibitory neurons reported here occur in a gradient extending out from the border of the LPZ. How do inhibitory neurons outside the LPZ sense the reduction MycoClean Mycoplasma Removal Kit of activity in the
LPZ? One possibility is that a reduction of input to layer 2/3 pyramidal cells located in the LPZ would lead to lower activity levels outside the LPZ by way of horizontal intracortical axon collaterals of these cells. Inhibitory neurons outside the LPZ would receive less excitatory input and react with a reduction of their spine and bouton density. What could be the possible function of a reduction in inhibitory structures outside of the LPZ? We speculate that reduced inhibition potentially acts as a signal to excitatory layer 2/3 cells in these regions to increase axonal sprouting within the LPZ, known to occur following lesions to facilitate functional reorganization (Darian-Smith and Gilbert, 1994 and Yamahachi et al., 2009). Consistent with this hypothesis, a recent study (Kreczko et al., 2009) demonstrated a decrease in GAD puncta on the somata of layer 2/3 excitatory cells following sensory deprivation, suggesting that a loss of inhibitory input to this specific group of cells does occur following input loss under at least some circumstances (but see Chen et al., 2011). Furthermore, Hu et al.
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