When most people think af the brain, they picture a lump of wrinkled grey matter. This part of the brain, known as the neocortex is only one part of the brain. However, the fold of the neocortex, which is only a few millimeters think, contain 70% of the cells in the brain. These cells are responsible for the highest level of cognition, including all thoughts as well as working and long-term memory ((1)).
Scientists have defined three unique types of memory. Working memory, which is processed in the prefrontal cortex coordinates long-term memories with sensory inputs ((1)). It allows us to keep a small amount of information active for a few seconds. It stores information needed only for a short time and provides a gateway to to long-term memory (). Long-term memory includes many things from one's knowledge of self the their understanding of how the world works. It is thought that long-term memory is processed in the hippocampus ((2), (3)). When a long-term memory is made, certain neuronal connections are strengthened, and others are weakend. These changes are fairly permanent, however some may take weeks or months before they are complete ((7)). Short- and long-term memory are grouped together and referred to as explicit memory because they both involve cognitive processes and in some cases concious thought to become established. A second category, implicit memory, is applied to a type of memory known as skill memory which does not require concious thought or control ((5)). Skill memory is processed in the cerebellum and then the information is passed the basal ganglia which store memories of this type and are also responsible for coordination and refining movement ((1)). However, amnesia is the clinical diagnosis only in cases where explicit memory has been damaged, so explicit memory will be the focus of the rest of this paper.
Without knowing precise mechanisms of how the brain works, scientists will never be able to completely explain the origins of amnesia. We do know that when traumatic brain injury occurs, the frontal and temporal lobes are almost always most severely damaged because of bone ridges in the skull associated with them. Brain cells may be killed or injured in the process. The brain does not regenerate dead nerve cells. Injured cells may or may not heal properly. When certain structures involved in processing and storing memory are damaged, amnesia sets in. In cases where the cells are reparably damaged or where other cells take over the functions of those killed, the amnesia will be temporary. In other cases, it is permanent ((8)).
Recent experiments and studies have begun to explain the mechanisms of amnesia and of memory itself. One of the most famous amnesia studies involves a patient referred to as H. M. H. M. was an epileptic who was incapacitated by his disease. In an attempt to relieve his seizures, the medial temporal lobe on both sides of his brain was removed. The surgery succeeded in relieving his seizures, but afterwards, the patient's short-term memory was severely damaged. Since that time, many experiments have been conducted in animal models using brain lesions as the source of head trauma. These studies have helped scientists to identify many structures in the brain which are associated with memory ((6)).
Another, more recent study has delved into the molecular rather than physiological processes involved in memory. Scientists have identified the cyclic AMP-response element binding protein (CREB). It seems to be an esential part of building long-term memories. A study in 1990 on sea slugs showed that nerve cells involved in memory storage are disturbed when a CREB disruptor is added. In another study, researchers showed that altering CREB protein and protein receptor levels alters the speed at which memories are formed. A group of rats who had their CREB levels altered solely in the hippocampus also showed a decline in long term memory, implying that CREB and the structures of the hippocampus somehow work together to process and/or store long-term memories. The research into CREB and related proteins also suggests a possible biochemical cause of amnesia along with the already established cause of head trauma ((9)).
Despite a vast amount of research into mechanisms of cognition and memory, we know almost nothing about the processes which occur in the neocortex. Coming research will surely show us more about the mechanism that store memories and that cause us to lose them. This research even raises the possibility of developing drugs or treatments for conditions like amnesia. Until that time, we will continue to be mystified by the mechanisms involved in memory and saddened and bewildered by it's loss.
2) Modulation of Memory Storage
5) Implicit and Explicit Memory
6) While You Were Sleeping: Recent Discoveries about Amnesia