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Abstract

In the past two decades there have been considerable advances in the understanding of the neural mechanisms of learning and memory in the mammalian higher brain. A preeminent view based upon the classical model of Hebb[27] holds that learning and memory may result from activity-dependent modifications of neural transmission at certain chemical synaptic junctions. Generally referred to as synaptic plasticity, such neuronal modifications are widely believed to occur in infancy and, to some extent, throughout adulthood. One of the best known examples of such synaptic modification is hippocampal long-term potentiation (LTP) of neural transmission which can be robustly induced by a brief period of tetanic (high-frequency) afferent stimulation, both in vivo and in vitro[3],[8],[9]. Recently, many other forms of synaptic plasticity have been identified in the hippocampus and other brain structures[4],[33],[37],[38]. it thus appears that synaptic plasticity is probably a generic property of many types of neurons which may be expressed throughout the mammalian central nervous system and may subserve a wide variety of neural functions.

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© 1996 Plenum Press

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Poon, CS. (1996). Synaptic Plasticity and Respiratory Control. In: Bioengineering Approaches to Pulmonary Physiology and Medicine. Springer, Boston, MA. https://doi.org/10.1007/978-0-585-34964-0_6

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  • DOI: https://doi.org/10.1007/978-0-585-34964-0_6

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