Synaptic plasticity describes the biological process that enables learning and memory through facilitating changes in the connections between synapses. Interaction with the external world results in synaptic activity, and patterns in this activity, both presynaptic and postsynaptic, can lead to changes in the connections between individual neurons, and ultimately, between neuronal networks.
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In essence, the continued use of particular synaptic connections facilitates their further use by strengthening their connection.
Changes at the level of the synapse support learning, memory, and more
Neuroplasticity plays a key role in numerous trademarks of human psychology. It allows for learning and memory to occur, it also allows experience to influence behavior, and it has been seen to play a role in both the development and treatment of certain psychological disorders. Cognitive-behavioral therapy, for example, is thought to work through taking advantage of neuroplasticity.
Neuroplasticity has also been implicated in the formation and maintenance of psychological disorders such as anxiety, depression, dementia, and even addiction. It is also thought to be essential to early brain development in children, as well as to recovery following brain injury.
Synaptic plasticity is essentially the process of neuroplasticity occurring at the single-cell level. It is the modification of neural circuitry through the malleability of the individual synapse. There is a large body of research that has elucidated the intricate workings of the synapse, uncovering how it makes modifications to the strength or efficacy of synaptic transmission as a response to stimuli, which may present itself in a myriad of forms).
These modifications of synaptic transmission result in stronger or weaker connections between individual synapses, which collectively add up to the effect of neuroplasticity.
Research has been able to provide insights into the underlying molecular mechanisms that allow synaptic modification to occur. Key mechanisms such as synaptic vesicle release and recycling, neurotransmitter receptor trafficking, and cell adhesion have all been implicated in synaptic plasticity, and an overview of their roles is given below.
Presynaptic mechanisms of [plasticity
In order to communicate with neighboring neurons, the presynaptic terminal of the synapse releases a neurotransmitter across the synaptic cleft, to be taken up by the postsynaptic receptor. The probability of the release of the neurotransmitter is controlled by a cytoskeleton matrix along with scaffolding proteins.
Synapsins are a family of phosphoproteins that influence the release of the neurotransmitter. Protein Kinases are activated through neuronal stimulation, which results in phosphorylation of the synapsins, which in turn modulate the tethering of synaptic vesicles, making them available for release.
So, synapsin phosphorylation is able to modulate communication between synapses. In addition, docking and priming are essential processes that allow synaptic vesicles to become fusion-competent. Studies have shown that RIM proteins are essential in regulating this process.
Postsynaptic mechanisms of plasticity
The release of the neurotransmitter from the presynaptic terminal is only part of the process that enables synaptic plasticity. The binding of the neurotransmitter to the postsynaptic terminal is also an essential part of the process. Research has found that the majority of postsynaptic principal neurons have dendritic spines, which accept the neurotransmitter.
Studies have proven that the number of these spines, along with their shape, changes during synaptic plasticity. These changes allow for stronger or weaker connections between specific synapses.
The level of intracellular calcium is essential in modulating postsynaptic activity. Increases in intracellular calcium within the postsynaptic compartment result in the activation of numerous downstream signaling enzymes. These enzymes have been seen to be essential in the regulation of synaptic plasticity.
Cell adhesion molecules are another essential factor in governing synapse plasticity. The space between the presynaptic and postsynaptic terminal, known as the synaptic cleft, is where the neurotransmitter crosses from the synapse of one neuron to the next. In addition, cell adhesion molecules are also found in this junction.
Research has uncovered that these molecules are responsible for keeping the two synapses close together, approximately 20 nm apart, with a force that is so strong it is impossible to separate the two synapses biochemically. Studies have shown that hippocampal learning tasks lead to an increase in levels of cell adhesion molecules in the synaptic cleft.
This highlights their role in synaptic plasticity, demonstrating that patterns in this activity (in this case, hippocampal learning) lead to their influx into the synaptic cleft, resulting in a stronger connection between the specific synapses.
Synaptic plasticity refers to the brain’s natural propensity to respond dynamically to stimuli. Brain activity initiates various processes that occur within and around the synapse, which results in it being more strongly or weakly connected to another. On a large scale, this results in slowly occurring changes to neural circuitry.
Due to its relation to learning and memory, as well as recovery from brain injury, and neuropsychiatric disorders, ongoing research into synaptic plasticity is essential in understanding the biological basis of key aspects of human psychology. It is essential for providing key insights into the difference between normal and pathological brain function.
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- Ho, V., Lee, J. and Martin, K. (2011). The Cell Biology of Synaptic Plasticity. Science, 334(6056), pp.623-628. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3286636/
- Fröhlich, F. (2016). Synaptic Plasticity. Network Neuroscience, pp.47-58. https://www.sciencedirect.com/science/article/pii/B9780128015605000045