Long-Term Memory

Long-Term Memory

There is no obvious demarcation between the more prolonged types of intermediate long-term memory and true long-term memory. The distinction is one of degree. However, long-term memory is generally believed to result from actual structural changes, instead of only chemical changes, at the synapses, and these enhance or suppress signal conduction. Again, let us recall experiments in primitive animals (where the nervous systems are much easier to study) that have aided immensely in understanding possible mechanisms of long-term memory.

Structural Changes Occur in Synapses During the Development of Long-Term Memory Electron microscopic pictures taken from invertebrate animals have demonstrated multiple physical struc-tural changes in many synapses during development of long-term memory traces. The structural changes will not occur if a drug is given that blocks DNA stimula-tion of protein replication in the presynaptic neuron; nor will the permanent memory trace develop. There-fore, it appears that development of true long-term memory depends on physically restructuring the synapses themselves in a way that changes their sensi-tivity for transmitting nervous signals.

The most important of the physical structural changes that occur are the following:

1.Increase in vesicle release sites for secretion of transmitter substance.

2.Increase in number of transmitter vesicles released.

3.Increase in number of presynaptic terminals.

4.Changes in structures of the dendritic spines that permit transmission of stronger signals.

Thus, in several different ways, the structural capa-bility of synapses to transmit signals appears to increase during establishment of true long-term memory traces.

Number of Neurons and Their Connectivities Often Change Significantly During Learning

During the first few weeks, months, and perhaps even year or so of life, many parts of the brain produce a great excess of neurons, and the neurons send out numerous axon branches to make connections with other neurons. If the new axons fail to connect with appropriate subsequent neurons, muscle cells, or gland cells, the new axons themselves will dissolute within a few weeks. Thus, the number of neuronal connections is determined by specific nerve growth factors released retrogradely from the stimulated cells. Furthermore, when insufficient connectivity occurs, the entire neuron that is sending out the axon branches might eventually disappear.

Therefore, soon after birth, there is a principle of “use it or lose it” that governs the final number of neurons and their connectivities in respective parts of the human nervous system. This is a type of learning. For example, if one eye of a newborn animal is covered for many weeks after birth, neurons in alternate stripes of the cerebral visual cortex—neurons normally con-nected to the covered eye—will degenerate, and the covered eye will remain either partially or totally blind for the remainder of life. Until recently, it was believed that very little “learning” is achieved in adult human beings and animals by modification of numbers of neurons in the memory circuits; however, recent research suggests that even adults use this mechanism to at least some extent.