Abstract
The present article discusses the anatomical and functional aspects of human memory. Memory is an integral part of our cognitive processes and gives the meaning to life. The importance of memory can be ascertained by studying the conditions associated with memory loss. Scientists have established the ‘what,’ ‘where’ and ‘how’ of the memory by using animal models or the modern computerized techniques like CT, MRI and PET. The medial temporal lobes of the hippocampal region are the primary sites of memory and learning. However, the final storage site of memory is presumed to be neo-cortex. Depending on the anatomical site involved, there can be different types of memories viz. Declarative and non-declarative memories. Several models for human memories have been proposed by the philosophers and researchers. The modal model proposed by Atkinson and Shriffin is one of the most popular models.
There are several internal and external factors that affect human learning and memory. A number of internal in-accuracies like forgetting, amnesia, degenerative diseases, etc. are responsible for partial or complete memory loss. Some of these in-accuracies are sudden while others are progressive. Memory enhancement is an area of interest for researchers as well as students. Memory enhancement techniques include the usage of chemical agents for increasing the attention, use of colors to enhance arousal as well as attention. Several other factors increasing the memory performance are discussed in the paper.
Memory is the ability of our brain to record and store the information and experiences. Memory makes it possible to hold the history and thereby aids in growth and change. ‘Learning’ and ‘remembering’ are the two pillars of memory and are central to the disciplines of biology, psychology and philosophy. Human race is continuously trying to improve its ‘understanding of the memory’ by answering the two key questions 1) where are memories stored? and 2) how are memories stored?
Memory plays a role whether or not we intend to learn. Each word we read and each sight we see change our memory in some way. The memory interprets these sensory inputs and fits the information in relation to previous knowledge. Memory also plays a role regardless of our intention to retrieve the events of the past. Many past influences pop into mind unexpectedly (Foster, 2009).
Types of memory
In the last quarter of twentieth century, it was recognized that memory can be of two types: Declarative memory and non-declarative memory. Both of these types are supported by different brain systems. Declarative memory is the capacity of brain to recollect the facts and events. It can be further classified into three types viz. Episodic memory, semantic memory and procedural memory. Episodic memory is the memory for the events experienced in life. This type of memory retains the details of date, time and situation related to a particular episode. Semantic memory is the memory of facts and concepts. It represents the knowledge that is retained irrespective of the circumstances (in which it was acquired). Procedural memory involves remembering a sequence of operations for doing/performing something. For example, riding of a bicycle involves remembering the procedure. Certain diseases like Parkinson’s disease preferentially affect procedural memory. The second broad class of memory is non-declarative memory. It represents a heterogeneous collection of non-conscious abilities including learning of skills, habits, etc. (Foster, 2009). Chart 1 presents the different types of memory.
Chart 1. Different types of memory.
Anatomical insights into memory
Human hippocampus is a small structure of the shape of a crooked pinkie finger and is placed under the cerebral cortex. It is a paired structure (one of each side of the brain) and the two hippocampi come near to joining at the back. The hippocampi lie on the inner sides of temporal lobes. The fimbria or fornix is a fiber pathway connecting the hippocampus to subcortical structures. Hippocampal region is the general term given to a set of medial temporal structures viz. Hippocampus, dentate gyrus, subiculum, entorhinal cortex and the fimbria (Gluck and Myers, 2001).
Much of the anatomical insights into the memory were provided by the establishment of animal model of human amnesia in monkey. Severe amnesia was noticed after bilateral surgical removal of medial temporal lobe. It was demonstrated that memory was a cerebral function and the lesions or surgical removal of the medial temporal lobe resulted in the impairment of declarative memory but did not affect non-declarative memory.
The role of hippocampus in memory and its impairment was further concretized by high resolution magnetic resonance imaging (MRI) studies. These studies revealed that in patients with circumscribed memory impairment, the hippocampal formation was reduced in size. Another technique, positron emission tomography (PET) was used to study the blood flow to the cerebral regions on normal healthy subjects while they completed words from three-letter stems. The largest area of activation in the memory was found to be posterior medial temporal lobe (hippocampal region) and parahippocampal gyrus. The other experiments done on monkey models concluded that hippocampus was the most important center for memory and even a partial damage to hippocampus was sufficient to induce memory impairment.
The damage to midline diencephalic region has also been linked with amnesia. The two structures that are most frequently implicated in the memory impairment are mammillary nuclei and medio-dorsal thalamic nucleus. Long term memory is associated with the transfer of information form neo-cortex to medial temporal lobe structures. Projections from the neocortex arrive in the parahippocampal cortex and perirhinal cortex. Further processing occurs in entorhinal cortex and hippocampal formation (dentate gyris, CA1 and CA3). Thus, we can conclude that medial temporal lobe and medial thalamic structures are required at the time of learning; however, these structures are not the repository for the permanent memory. The slow-developing permanent memory is established in the neo-cortex (Zola-Morgan and Squire, 1993).
Models and mechanisms of memory
Numerous models of memory have been proposed by scientists and philosophers. Plato presented the memory as a wax tablet, on which impressions are encoded. According to Plato, these impressions were then stored and received as and when needed. Therefore, the encoding, storing and retrieving are the three processes taking part in the memory function.
Modern scientists claim that memory is not a passive storage of information. They see memory as a combination of selective and interpretive process. According to this view point, after learning and storing, human mind can interpret and integrate one thing with other so as to make better use of what is learnt and remembered (Foster, 2009). One of the most popular models of human memory is multi-store model or modal model. It was proposed by Richard Atkinson and Richard Shiffrin in 1968. This model states that there are three components of the memory: 1) Sensory component, 2) short term store and 3) long term store. Sensory memory is associated with sensory systems and these systems (vision, touch, etc) detect the sensory stimulus from the environment. A sensory memory register is created and the information from this register is transferred to short-term memory when the attention is given to it (otherwise it decays rapidly). Some of the useful information from the sensory memory is transferred to short-term memory (also called working memory). The information in the working memory is represented by a pattern of neural activity in the brain and is subsequently stored. Long term memory is the permanent memory in which we hold information even when we are not consciously attending to it. Information in the long-term memory is not represented by patterns of neural activity (as in short-term memory), rather it changes the conductivity of existing synapses. It may lead to the formation of new synapses and the destruction of the old synapses.
This model relies heavily on the rehearsal of information and rehearsal is the key process for the transfer of information from short-term to long-term memory. However, the experience shows that subjects do not actually rehearse the data that is actually stored. Another limitation of this model is that it presents the brain as a rigid structure of compartments (for sensory, short-term and long-term memories). However, the brain that process and store the information in parallel. Hence, the compartments do not really exist (McLeod, 2007).
Inaccuracies of the memory
Forgetting: It is defined as the complete or partial loss of information that was stored. Forgetting may result when the memories fade or decay with time. Forgetting may occur when memory traces are disrupted or overlaid by other memories.
Amnesic syndrome: It is an example of memory impairment due to brain injury (involving hippocampus and diencephalon). In this syndrome, the patient exhibit anterograde and retrograde amnesia. Anterograde amnesia is the loss of memory for information that occurred after the brain injury and retrograde amnesia is the loss of memory for information that occurred before the injury.
Psychogenic amnesia: It is the impairment of memory without any evidence of neurological brain injury. This type of amnesia is experienced by the people in dissociative state (when they are partially or wholly separated from their memories) due to certain shocks (like witnessing a murder, an accident, etc.) (Foster, 2009).
Alzhiemer’s & other degenerative diseases: It is a type of dementia that causes problems with memory, thinking and behavior. It is a progressive disease and memory loss increases with the severity of the disease. The most common early symptom of Alzhiemer’s disease is difficulty in remembering the new information.
Herpes encephalitis: It occurs when the herpes virus enters the brain and attacks nerve cells. It results in the decrease in the level of consciousness and altered mental state of confusion. The electrical activity of the brain changes with the progression of the disease. CT and MRI scans present the abnormalities in temporal lobes of the brain.
The other factors impairing learning and memory are autism, dyslexia, old age, Parkinson’s disease, physical brain injury etc.
Improving the memory
With the current scientific knowledge, we cannot improve the ‘biological hardware’ involved in the memory. However, certain chemical agents can enhance the memory by improving the attention. For example, the agents like caffeine and nicotine are known to stimulate our cognitive system. These agents increase the chemical transmission or communication between the brain cells. These are not helpful in restoration of the memory after brain damage or illness (dementia).
We can focus of the ‘biological software’ for the improvement of the memory. Effective learning techniques like repetition, mental mapping and coding significantly enhance the memory (Foster, 2009). Researchers have shown that physical exercise increases oxygen to the brain and reduces the risk of memory impairment and related disorders. A good night’s sleep is another memory-enhancing activity. It enhances problem-solving capabilities and critical thinking skills. Continuous mental stress may lead to the damage of the hippocampus, an area of the brain involved in memory and learning. Hence, it is advisable to relax and boost the emotional health. Meditation is another very important technique for the enhancement of memory.
Influence of color: Colors constitute important visual experiences in human beings and have a significant role in enhancing memory performance. Colors are reported to increase the attention and arousal to the environment. Vivid color cues enhance the short-term memory performance in Alzheimer’s disease (Dzulkifli and Mustafar, 2013).
Mnemonic devices: Mnemonics like visual images, acrostics and rhythms, etc. are the clues that can help in remembering something.
Mechanism-Based Drugs: Owing to the knowledge of synaptic changes occurring during memory encoding, it is now possible to build the memory-enhancing drugs. These drugs act on distinct cellular targets and increase the memory retention in a number of species (Lynch, 2002).
References
Dzulkifli, M. A. & Mustafar, M. F. (2013). The influence of color on memory performance: Review. Malaysian Journal of Medical Sciences, 20(2), 3-9.
Foster, J. K. (2009). Memory: A very short introduction. New York: Oxford University Press.
Gluck, M. A. & Myers, C. E. (2001). Gateway to memory. Cambridge: The MIT Press.
Lynch, G. (2002). Memory enhancement: The search for mechanism-based drugs. Nature Neuroscience, 5, 1035-1038.
McLeod, S. (2007). Multi-store model of memory- Atkinson and Shriffin, 1968. Simply Psychology. Retrieved from http://www.simplypsychology.org/multi-store.html
Zola-Morgan, S. & Squire, L. R. (1993). Neuroanatomy of memory. Annual Reviews in Neuroscience, 16, 547-563.
