Cellular and Molecular Changes in Associative Memory

Abstract

Basic units in the brain include neurons, glia cells, and their synaptic connections. Neuronal codes for the execution of various brain functions, such as memory, cognition, and emotion, are programmed by these neurons and synapses. While acquiring exogenous signals and processing endogenous signals, these signals are memorized in the brain essentially for guiding cognitions and behaviors. Memory formation and memory-relevant behavior emergence may be based on the recruitment and/or refinement of these neurons and synapses. The recruitment of neurons to be the basic units in memory traces will be discussed in Chap. 5. Here, author intends to summarize the plasticity of neurons and synapses, which is presumably relevant to memory formation. The featured function of neurons is to produce action potentials, or spikes, once excitatory synaptic signals drive their membrane potentials to a threshold potential for firing spikes or their membrane potentials fluctuate to this threshold potential. The patterns of neuronal spikes constitute the digital signals to program various signals and manager neuronal functions. In this regard, the plasticity at neurons is mainly characterized by changes in their spike patterns and/or threshold potentials that may move closely or away from the resting membrane potential. In terms of chemical synapses, their signal transmission includes transmitter release from presynaptic boutons as well as interactions between transmitters and their receptors in postsynaptic density. The plasticity at chemical synapses includes the changes in the capacity and release efficacy of presynaptic transmitters as well as in the number and responsiveness of postsynaptic receptors, which may control the conversions between inactive synapses and active synapses or between silent synapses and functional synapses. Long-term plasticity at synapses and neurons is believed to be cellular mechanisms underlying memory formation, which leads to long-term changes in memory-relevant behaviors.