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Homosynaptic Plasticity


Homosynaptic plasticity is one type of synaptic plasticity. Homosynaptic plasticity is input-specific, meaning changes in synapse strength occur only at post-synaptic targets specifically stimulated by a pre-synaptic target. Therefore, the spread of the signal from the pre-synaptic cell is localized.

Another type of synaptic plasticity, heterosynaptic plasticity, is not input-specific and differs from homosynaptic plasticity in many mechanisms.

In addition to being input-specific, the strengthening of a synapse via homosynaptic plasticity is associative, because it is dependent on the firing of a presynaptic and postsynaptic neuron closely in time. This associativity increases the chances that the postsynaptic neuron will also fire. These mechanisms are used primarily for learning and short-term memory.

Donald Hebb theorized that strengthening of synaptic connections occurred because of coordinated activity between the pre-synaptic terminal and post-synaptic dendrite. According to Hebb, these two cells are strengthened because their signaling occurs together in space and/or time, also known as coincident activity. This postulate is often summarized as Cells that fire together, wire together, which means that the synapses that have neurons with coincident firing are strengthened, while the other synapses on these neurons remain unchanged. Hebb's postulate has provided a conceptual framework for how synaptic plasticity underlies long-term information storage.

Changes in plasticity often occurs via the insertion or internalization of AMPA receptors (AMPARs) into the postsynaptic membrane of the synapse undergoing a change in connective strength. Ca2+ is one signaling ion that causes this AMPA receptor density change by inducing a cascade of biological changes within the cell. To induce long-term potentiation (LTP), Ca2+ activates CAMKII and PKC, causing phosphorylation and insertion of AMPARs, while long-term depression (LTD) occurs by Ca2+ activating protein phosphatases, which dephosphorylate and cause internalization of AMPARs.

In order to create input-specific changes in synaptic strength, the Ca2+ signal must be restricted to specific dendritic spines. Dendritic restriction of Ca2+ is mediated by several mechanisms. Extracellular Ca2+ can enter the spine through NMDA receptors (NMDARs) and voltage gated Ca2+ channels (VGCCs). Both NMDARs and VGCCs are concentrated on dendritic spines, mediating spine specific Ca2+ influx. Intracellular stores of Ca2+ in the endoplasmic reticulum and mitochondria may also contribute to spine restricted signaling, although some studies have failed to find evidence for this. Clearance of Ca2+ is controlled by buffer proteins, which bind to Ca2+ and keep it from trickling out to other spines. Restricted diffusion of Ca2+ across the neck of the dendritic spine also helps isolate it to specific dendrites.


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