g. see Holland & Petrovich, 2005; Yin et al., 2008). This effort might be aided by multisite recordings or targeted online manipulations of key firing patterns to causally control PIT, as
well as task designs to dissociate general from outcome-specific forms of PIT (Blundell et al., 2001; Corbit & Balleine, 2005). For now, however, this work represents an important and ‘motivating’ step forwards. “
“An emerging DAPT molecular weight view of structure–function relations of synapses in central spiny neurons asserts that larger spines produce large synaptic currents and that these large spines are persistent (‘memory’) compared to small spines which are transient. Furthermore, ‘learning’ involves enlargement of small spine heads and their conversion to being large and stable. It is also assumed that the number of spines, hence the number of synapses, is reflected in the frequency
of miniature excitatory postsynaptic currents (mEPSCs). Consequently, there is an assumption that the size and number of mEPSCs are closely correlated with, respectively, the physical size of synapses and number of spines. However, several recent observations do not conform to these generalizations, necessitating a reassessment of the model: spine dimension and synaptic responses are not always correlated. It is proposed that spines are formed and shaped by ongoing network activity, Alpelisib cell line not necessarily by a ‘learning’ event, to the extent that, in the absence
of such activity, new spines are not formed and existing ones disappear or convert into thin filopodia. In the absence of spines, neurons can still maintain synapses with afferent fibers, which can now terminate on its dendritic shaft. Shaft synapses are likely to produce larger synaptic currents than spine synapses. Following loss of their spines, neurons are less able to cope with the large selleck chemicals synaptic inputs impinging on their dendritic shafts, and these inputs may lead to their eventual death. Thus, dendritic spines protect neurons from synaptic activity-induced rises in intracellular calcium concentrations. It has been postulated that dendritic spines underlie the neuronal locus of plasticity, in which long-term alterations in synaptic strength (‘memory’) are converted into persistent morphological changes. While ongoing studies attempt to characterize the nature of these morphological changes and the molecular cascades leading to them (Bhatt et al., 2009; Yoshihara et al., 2009; Holtmaat & Svoboda, 2009; Yang & Zhou, 2009; Segal, 2005), it is still not clear what constitutes a ‘memory’ at the spine level, if at all such a function can be assigned to a single dendritic spine. One major issue is whether spine morphology follows changes in ambient network activity, or does it genuinely store ‘memory’ which can be formed even after a single association between two neurons firing, irrespective of the ongoing background activity.
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