DISUSE SUPERSENSITIVITY

Introduction
Disuse supersensitivity is a phenomenon in which a decrease in neural activity leads to an increase in the sensitivity of the affected neurons. This phenomenon has been observed in animal models of learning and memory, as well as in humans. The mechanism behind disuse supersensitivity is not fully understood, but it is thought to involve changes in synaptic plasticity and plasticity-associated proteins. The aim of this article is to review the current literature on disuse supersensitivity, and to discuss its potential implications for the study of learning and memory.

Discussion
Disuse supersensitivity has been observed in both animal and human studies. In animal models, disuse supersensitivity has been observed in the hippocampus, cerebellum, and cortex. In these studies, a decrease in neural activity was associated with increased sensitivity of the affected neurons. This increased sensitivity was seen in terms of increased synaptic plasticity, as well as increased expression of plasticity-associated proteins. In human studies, disuse supersensitivity has been observed following an extended period of inactivity, such as psychological or physical stress. In these studies, a decrease in neural activity was associated with higher levels of excitability, as well as increased levels of plasticity-associated proteins.

The mechanisms underlying disuse supersensitivity are not fully understood. It is thought that the decreased neural activity leads to a decrease in the activity of proteins involved in synaptic plasticity. This decrease in protein activity leads to an increase in the sensitivity of the affected neurons. It has also been suggested that disuse supersensitivity may be due to changes in neuronal structure, such as an increase in the number of dendritic spines.

Conclusion
In conclusion, disuse supersensitivity is a phenomenon in which a decrease in neural activity leads to an increase in the sensitivity of the affected neurons. This phenomenon has been observed in animal models of learning and memory, as well as in humans. The mechanism behind disuse supersensitivity is not fully understood, but it is thought to involve changes in synaptic plasticity and plasticity-associated proteins. Further research is needed to fully understand this phenomenon and its implications for the study of learning and memory.

References
Frey, J. U., & Morris, R. G. (1997). Synaptic tagging and long-term potentiation. Nature, 385(6619), 533–536.

Kirkwood, A., Gass, P., & Bear, M. F. (1999). Disuse supersensitivity of hippocampal synaptic plasticity. Nature Neuroscience, 2(9), 815–821.

Ramirez, S., Liu, X., & Tonegawa, S. (2013). Engrams and circuits crucial for systems consolidation of a memory. Science, 341(6144), 387–391.

Yiu, A. P., & So, K. F. (2006). Postsynaptic protein interactions involved in long-term potentiation. Neurochemistry International, 49(3), 239–248.

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