Published online by Cambridge University Press: 05 August 2016
Memory comprises the recording, retention and retrieval of knowledge. All that we know, except for what is genetically predetermined, is acquired through experience. Such knowledge includes the events we remember, the facts we know, and the skills we master. Memory is not a unitary faculty, but rather an ensemble of multiple forms of learning that differ in their uses, their operating characteristics, and the neural networks that mediate their processing (Gabrieli, 1998). A memory system may be defined as a particular neural network that mediates a specific form of mnemonic processing. Neurological and psychiatric diseases result in characteristic mnemonic deficits that reflect which memory systems are injured by a particular disease.
Levels of analysis: cells and systems
Learning and memory reflect experience-induced plasticity in the brain. An experience leaves a memory trace composed of an enduring alteration in the cellular organization of the brain called an engram. Experience-induced plasticity can be examined at many levels of analysis, including molecular events at the cellular and synaptic level, reorganization of local neuronal circuits, and large-scale alterations in the functional neural architecture of memory systems.
Cellular mechanisms of memory
Little is known about neural plasticity in the human brain, but findings from in vitro and invertebrate models offer suggestions about the cellular bases of human memory. Studies of the marine snail Aplysia have revealed links between learning and alterations in neurotransmitter release. Aplysia have a gill withdrawal reflex that is triggered when the gill is touched by a rod. Repeated stimulation leads to habituation such that the gills are no longer withdrawn in response to the rod. Short-term habituation has been linked to decreased presynaptic transmitter release. Repeated stimulation with a highly noxious stimulus, such as an electric shock, can lead to sensitization, an intensification of the withdrawal response. Short-term sensitization involves increased neurotransmitter release from a facilitating interneuron (Kandel & Schwartz, 1982). Modulation of neurotransmitter release may underlie short-term changes in functional connectivity between neurons.
Long-term memory processes, in contrast, require messenger RNA and protein synthesis (Davis & Squire, 1984) to establish structural changes in synaptic connectivity as a record of experience.