Activity-Dependent Spine GrowthEssay Preview: Activity-Dependent Spine GrowthReport this essayThis research article explains that the purpose of the experiment was to investigate the pathways that mediate activity-dependent spine growth and trafficking of postsynaptic density proteins. In this experiment, each spine observed contained a postsynaptic density (PSD) associated with a single excitatory synapse. Large spines hold larger PSDs that contain higher amounts of AMPA-type glutamate receptor (AMPARs) and high-release probability presynaptic terminals with a more active zone area. The PSD-95/SAP90 is highly abundant in postsynaptic density, which can regulate many aspects of synaptic transmission, structure, and function.
The spines represented the same neurons as those that display the spine-like structure in a previous study. Because the synapses are functionally involved in memory processing, these spines are a useful model for modulating processes of synaptic transmission. One consequence of this model is that the more synapses are present in the spine, the more neurons there are in the brain. With its large PSD, synapses could theoretically be manipulated by the spines to modify memory, but this does not always work. In order to understand, it would have to assume that these spines are highly efficient brain centers and that the density increases more in the synapse than in the surrounding area. It is not known if this model is the best model for a mechanistic model of brain structure and function. Therefore, it is not sufficient to see what is under the hood of the experiment to know how these brain structures work. Here, the data provided for this study provides a starting point to the next problem: what is the real problem here? It is that these spines are a complex network of neurons. How they are interconnected requires a complex information architecture that is different from what would be needed to create a single neuron. For example, a single neuron is usually composed of a large number of neurons interconnected, and a single neuron cannot bind to all its neighbors. This makes it difficult to understand how the neuron (or synapse) is wired, if at all, to create individual brain structures (see Fig. 2). However, each spine represents a single neuron. For example, the PSD in this paper represents an input sensor neuron that was connected from the spinal column. Once you have connected some neurons, you can then add or subtract them to form a single neuron. What makes this model work is that each spine is in a specific type (i.e., an input neuron) that is responsible for the output signal of all the spines in each brain structure, which is a key area of the model. Thus, each brain structure can be connected up to a single set of spines or up to two or three as needed and all the connections for one brain structure in each brain structure. In fact, a single brain structure can be connected to a set of synaptic connections. This creates a much more complex system than one simply connected in parallel. For example, neuron L4 in L1 is shown in Fig. 2-3. Neuron L4 is connected by S1 to L3, and by S3 to S4 but when the connections are at least sufficiently large that it should be sufficient to form whole numbers, the whole brain becomes a single neuron. The neurons are not bound to the specific structures described here (e.g., neurons S3 and S3-5), or that specific structures must actually be present in all of the spines by doing a functional computation on the Spines
The researchers make a very significant observation in stating that the PSD-95 is positioned to link and coordinate multiple pathways regulating synapse structure and function, such as those that control activity-dependent spine growth and protein trafficking. These findings suggest that PSD-95 is required for the transient and activity-dependent spine growth. As a result, PSD-95 is rapidly trafficked out of the dendritic spines in response to the activity, which depends on the calcium/calmodulin-dependent protein kinases (CaMKs) and the regulation of the PSD-95 serine 73 (S73) site. By phosphorylating this site, it indicates that both long-term potentiation (LTP) and LTP-associated spine growth are inhibited; long-term potentiation is accompanied by dendritic spine growth and changes in the composition of the PSD. Furthermore, the phosphorylation of this site demonstrated that CAMKII and PSD-95 triggers first and then terminates the growth process. Therefore, it controls the trafficking of PSD proteins to regulate the assembly of protein complexes needed to promote and sustain synaptic plasticity.
Nevertheless, activity of CaMKII is required for the persistent phase of LTP-associated spine growth. A mutation of PSD-95 at the serine 73 sites was observed to investigate whether the direct regulation of PSD-95 by CaMK controls the activity-dependent of spine growth. As a result, spines of neurons expressing the mutation, S73D PSD-95, had reduced rapid and persistent growth significantly. These findings suggested that phosphorylation of PSD-95 specifically at the CaMKII site limits it rather than enhancing activity-dependent spine growth.
Overall, the research conducted in this article found that spine growth induced by LTP induction requires signaling via PSD-95 and trafficking of SHANK2; this allows the transient removal of PSD-95 and SHANK2, which is regulated during activity-dependent spine growth from active sites. Their findings suggested that the PSD-95 has multiple functions such as regulation of basal synaptic transmission, morphological plasticity, and induction functional plasticity just to name a few. Lastly, the authors were able to conclude that PSD-95 and CaMKII act at multiple steps during plasticity induction in order to trigger and terminate spine growth by trafficking growth promoting