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Concepts of Memory

The chapter opens by defining learning and memory. Their neurophysiological basis is explained. A strong emphasis is placed on the role played by modification of the synapse, the point of communication between neurons. It is shown how this process of modification underpins neural plasticity and may facilitate learning and memory.

There is a brief overview of the history of memory theory. It is shown, in particular, that the work of some early theorists in this field, such as James and Bartlett, fits well with some occupational therapy concepts. There is also a discussion of the 'cognitive revolution' that took place in psychology in the United States in the 1950s. Some practical applications of the 'information processing' turn that this involved are explained.

The chapter also contains a detailed description of the case of Henry Molaison. This is justified by the far-reaching implications of these findings for learning and memory theory. Following from this, space is devoted to a detailed discussion of the 'hippocampal memory system'.

Some leading theorists have developed models of memory. The chapter includes a detailed discussion of Tulving's hierarchal model of procedural, semantic and episodic memory. In addition, there is consideration of the 'multicomponent working memory' model, which is particularly associated with the work of Baddeley. Also, there is discussion of the concept of prospective memory and reflection on the work of Luria and Vygotsky on the socio-historical origins of cognitive processes.

Defining Learning and Memory

The learning process allows the acquisition of novel information (Gazzaniga et al. 1998, 2009). Memory is the persistence of this learned content in a condition in which it can be retrieved in the future (Gazzaniga et al. 1998, 2009; Schacter and Wagner 2013). This linkage means that scientific accounts have often discussed learning and memory in combination (Tulving and Madigan 1970; Gazzaniga et al. 2009).

Memory's role in occupation has been explored by occupational therapy theorists including Hagedorn (2000, p. 31), who defined it as a 'skill component' of performance, and Radomski (2002, p. 198), for whom it was a 'primary cognitive capacity' underpinning 'higher level thinking abilities'. Kielhofner (2008, p. 18), meanwhile, described memory as an aspect of cognition that could support 'performance capacity'. For all these authors memory, then, is fundamental to effective occupational performance.

For Kandel et al. (2000), learning and memory are the supreme processes through which the environment influences our behaviour. So, learning and memory formation imply a change in the organism at some level and this requires both stable body structures and the capacity to modify these in response to experience (Kielhofner 1995; Rose 1992). The persistent stability of the organism is called 'specificity'; the ability to change, 'plasticity' (Rose 1992, p. 137).

These themes of change and stability have also been discussed by occupational therapy theorists. Kielhofner (1995, p. 10), for example, drew on 'general, dynamical and open systems theories' in his examination of human occupation. A system is made up of components that function in concert for a specified purpose: an 'open system' constantly changes and organises itself as it interacts with its environment, while 'dynamical systems' describe the process by which a novel order emerges following an epoch of flux (Kielhofner 1995, p. 9). In the following section, these themes are explored in relation to learning and memory from within a 'physiological frame of reference' (Hagedorn 1992).

Neurophysiological Mechanisms of Learning and Memory

In order to understand the 'organic substrate' (Trombly 2002, p. 7) that allows the changes brought about through learning to take place while maintaining the continuity of the organism, it is first important to grasp that communication within the nervous system requires the transfer of information between neurons (Bear et al. 2016). Neurons are nerve cells that possess electrical excitability and underpin functions such as learning and memory (Tortora and Derrickson 2011). Communication between neurons occurs at sites called synapses, where a presynaptic neuron signals to a postsynaptic neuron; typically, the 'presynaptic element' is the terminal ending of an axon, while the postsynaptic component is a dendrite on the postsynaptic neuron (Bear et al. 2016). This communication is discussed in more detail later in the chapter.

In most synapses, the presynaptic and postsynaptic neuronal membranes are separated by a microscopic gap, the synaptic cleft (Bear et al. 2016). The presynaptic axon terminal houses 100-200 microscopic spheres named 'synaptic vesicles' that contain chemicals called neurotransmitters, the medium of communication between the neurons (Bear et al. 2016; Siegelbaum and Kandel 2013). Vesicles release their neurotransmitter into the synaptic cleft in response to an electrical signal called an action potential, or nerve impulse, travelling to the axon terminal of the presynaptic neuron (Bear et al. 2016; Siegelbaum and Kandel 2013; Tortora and Derrickson 2011). The neurotransmitters bind to receptor sites on the postsynaptic neuron; these sites are normally closed, but they open when particular neurotransmitters cleave to them (Bear et al. 2016). The synaptic cleft, then, is the region of communication between the pre- and postsynaptic neurons.

The receptor sites are located on channels in the postsynaptic cell membrane. When neurotransmitters bind to these sites, the channels open. The channels are specialised to permit only certain ions to enter or exit the cell (Bear et al. 2016; Tortora and Derrickson 2011). Ions are atoms or molecules with an electrical charge, conventionally labelled as either 'positive' or 'negative', meaning that they can cause a force of attraction or repulsion when close to another ion. The movement of these ions creates a current across the cell membrane, with implications that are explained later.

The ions that cross the postsynaptic membrane enter from the extracellular fluid and cause changes in the voltage of the membrane of the postsynaptic neuron (Bear et al. 2016; Tortora and Derrickson 2011). Voltage is a measure of the difference in electrical energy between two locations, in this case between the outer membrane and inner membrane of the neuron. The difference is created as a result of the varying amounts of negatively and positively charged ions on either side of the membrane. This difference results in a membrane potential, typically of -70?mV, a value indicating that the inner membrane of the neuron is negatively charged when compared with the outer membrane (Gazzaniga et al. 2009). As already stated, the neuron is electrically excitable, meaning that the membrane potential can change as a result of a stimulus, so this value is named the resting membrane potential (Martini 2018). The resting membrane potential, then, can change as result of ions entering the neuron.

Sodium ions have a positive charge, so if sodium ion channels open and these ions enter the postsynaptic cell, they cause an increase of positive charge in the region around the cell's inner membrane (Tortora and Derrickson 2011). This leads to a reduction in the negativity of the membrane potential, a phenomenon labelled depolarization (Siegelbaum and Kandel 2013; Bear et al. 2016). If potassium ion channels open, leading to an outflow of these positively charged ions, this leads to a rise in negative charge at the inner cell membrane, resulting in an increase in the negativity of the membrane potential, a phenomenon labelled hyperpolarisation (Tortora and Derrickson 2011). The opening of chloride channels will lead to an inflow of these negatively charged ions, also leading to hyperpolarisation (Tortora and Derrickson 2011).

These variations in the membrane potential make it more or less likely that an action potential, also called a nerve impulse, will be generated. The action potential is an electrical signal that conducts along the axon of the neuron without losing strength, a process called propagation (Tortora and Derrickson 2011). As already shown, once the action potential reaches the axon terminal it causes neurotransmitter to be released into the synaptic cleft, so that interneuronal communication can occur. If hyperpolarisation occurs in the postsynaptic neuron, this results in an inhibitory postsynaptic potential, meaning that an action potential will not be generated (Siegelbaum and Kandel 2013; Bear et al. 2016). However, when depolarisation occurs in the postsynaptic neuron, there will be an excitatory postsynaptic potential (Siegelbaum and Kandel 2013; Bear et al. 2016). If the excitatory postsynaptic potential results in a change in the membrane potential to a threshold value of -55?mV, then an action potential will be generated (Tortora and Derrickson...