SHORT TERM MEMORY LONG TERM MEMORY AND THE BRAIN

In this vein, there are different areas associated with specific memory subsystems (Squire & Zola, 1997). This paper seeks to explore the regions of the brain liable for short-term memory and long-term memory and how these areas affect memory as a result of damage and dysfunction. Also referred to as primary memory, short-term memory is the faculty for grasping little bits of information in mind in an active, readily accessible condition for a short time, usually in the order of seconds (Baddeley, 2017). Additionally, the capacity for short-term memory is limited. According to Miller (1956), this type of memory can store seven-two more or less, items, and thus called this concept the magic number 7. These structures, according to them are the central executive, visuospatial sketchpad, and the phonological loop, each independent of the other.

The central executive plays a supervisory function on the kind of items that enter and exit the systems. Also fundamental for navigation, the visuospatial sketchpad processes and saves information in a visual and spatial mode. An illustration for this subsystem is that information is updated continuously as we navigate our environment since our positions concerning objects keep changing. The phonological loop handles written and spoken data. This region acts a temporary store of information as it is being used for present reasoning processes (Gloor, 1997). Miller and Cohen (2001) hold the view that information relevant to a specific task is encoded in the prefrontal cortex. Multiple imaging techniques have been applied to prove this fact. For instance, intense neural activity was observed in the prefrontal cortex during the working memory tasks’ delay period.

The delay periods activity was found to encompass two components that it is specific to the stimulus being remembered, and that task-relevant information is encoded, showing resistance to distractors. Transferring data to the long-term memory for permanent storage occurs when there is mental repetition or rehearsal of the information, or giving the information meaning and relating it to previously acquired knowledge (Baddeley, 2017). An experiment done by Murdock (1962) shows the distinction between short-term memory and long-term memory in regards to encoding, duration, and capacity. Murdock asked participants to learn and free recall a list of words that were different in length. He noticed that the possibility of recalling a word depended on its position on the list (Murdock, 1962). Words in the middle of the list were easily forgotten while those at the beginning or end of the list were easy to recall.

Long-term memory can be classified into explicit memory and implicit memory (Squire & Zola, 1998). Declarative memory, also explicit memory represents memories that are available in the conscious. Additionally, it can be separated into episodic memory, semantic memory, and autobiographical memory. Episodic memory is responsible for formation and retrieval of the memory of particular events in time such as remembering a person’ name and the circumstances surrounding previous interactions with them. Semantic memory, on the other hand, is involved with knowledge on facts like word meaning and understanding about the world (Squire & Zola, 1997). For example, how to hold a crayon, ride a bicycle, or skip a rope (Parkin, 2016). Evidently, this kind of memory is supposedly saved by the striatum and additional segments of the basal ganglia after encoding.

The basal ganglia are considered to act as a link between procedural memory and structures in the brain and are virtually independent of the hippocampus. According to studies performed by Wood et al. (2000), it was discovered that there is a connection between implicit memory and the revival of the parietal and occipital regions of the brain. One of the famous cases studied by scholars on amnesia is that of H. M. , whose hippocampus was consensually taken out as a measure to remedy epilepsy (Catani et al. Due to this treatment, he developed amnesia thus preventing him from creating new long-term memories. For instances, after previously engaging in a conversation with a person, he would have no recollection of having met them.

Korsakoff’s syndrome, which results from impairment or injury to the dorsomedial thalamus as a result vitamin insufficiency is also a likely occurrence to memory deficit. The main symptoms of this syndrome are retrograde and anterograde amnesia and false memories which are adapted to be true, also known as confabulation. Notably, this is evident because analyses of structural magnetic resonance imaging depict that there is a close association between the medial temporal lobe and the diencephalon and are often considered to be a single functional structure (Gloor, 1997). Besides damage to the thalamus, Korsakoff’s syndrome results from impairment of the mammillary bodies of the hypothalamus and also damage to neurons (Squire & Zola, 1997). With these data from studying cases of amnesia, it is imperative to think about the dynamic role of these brain structures.

Markedly, this means that he experienced severe amnesia and an incapacity to form new memories such as time and place that an event occurred. However, the retained memories of earlier years dating back to childhood (Squire & Zola, 1998). In another case of acquired amnesia reported in 1987 by Ostergaard, a ten-year-old lad developed amnesia after an episode of anoxia (Gloor, 1997). Consequently, this resulted in multifocal brain damage encompassing regions of the hippocampus bilaterally. Even though procedural memory and overall intelligence remained intact, proof of shortfalls declarative memory, mainly semantic and episodic memory, remained. In regards to understanding the explicit memory from hippocampal patients, difficulties in making conclusions have been experiences. Notably, this is because of differences in the sizes of lesions under study, dissimilarities in how these lesions came about, a difference in patient’s ages, and variations in testing methods.

For instance, in the case of HM, his short-term memory remained intact while impairment in long-term memory was observed. Also, symptoms of anterograde amnesia were seen while past events before the surgery were still recalled. Markedly, this shows that there is a difference between anterograde amnesia and retrograde amnesia. One of such tasks was exercise, mainly running. Two groups of mice were used to test this hypothesis. One was assigned to running after being put in a cage containing a running wheel. MR brain images showed the generation of more neurons to the mice that exercised compared to those that did not (Spalding et al. Contrary to this study, another research was conducted on fifty-four participants across the age spectrum to reveal that adults do not generate new brain nerve cells necessary for memory and navigation (Sorrells et al.

Thus, using projection to the posterior zones, the dorsolateral prefrontal cortex maintains the activity in sensory regions to enable them to be retained in memory. Long-term memory is therefore rebooted into working memory by frontal protuberances to the lateral anterior temporal lobes. In regards to this explanation, patients with damage to the frontal lobe portray deficits in both concentration and maintaining attention hence a poor working memory but support excellent explicit recognition memory. A poor recall is exhibited in frontal patients. Notably, this has further been explained to be a result of deficient search and retrieval strategies that portray the incapacity to obstruct extraneous associations of memory (Van et al. Often, this regulation is made possible by stress hormones. A memory trace may be formed as a result of increased arousal and blood sugar levels in the presence of a stress hormone.

These hormones on their own have been observed to contribute to the modulation of memories. The amygdala performs an essential function in the encoding of emotional memory. In this vein, aversive conditioning relies on this region of the brain (Jin & Maren, 2015). Baddeley, A. D.  Working memory. Oxford: Oxford University Press. Baddeley, A. , Dell’Acqua, F. , & De Schotten, M. T. A revised limbic system model for memory, emotion and behaviour.  Neuroscience & Biobehavioral Reviews, 37(8), 1724-1737.  Behavioural brain research, 199(1), 53-60. Miller, E. K. , and Cohen, J. D. B. Direction of recall in short-term memory.  Journal of Verbal Learning and Verbal Behavior, 1(2), 119-124. Parkin, A. J. , & Milner, B. Loss of recent memory after bilateral hippocampal lesions.  The Journal of neuropsychiatry and clinical neurosciences, 12(1), 103-a. Sorrells, S.