We remember more than we know, although the normal traffic of action potentials in the brain doesn’t leave permanent traces. We don’t want to remember most of our experiences, anyway. (When was the last time you burped?) When something important does happen, though, it gets fast-tracked into long-term memory, to be held for years of systems consolidationand repeatedly reconsolidated.
The fast-track consolidation occurs at the synaptic level. It is called long-term potentiation, or LTP. It works in conjunction with an opposing process, long-term depression, or LTD. When a rapid series of action potentials is fired into the hippocampus from outside the structure, cells within the hippocampus increase their own activity. For a long time afterwards—hours, days, weeks—those neurons will continue to fire with high sensitivity to just normal input activity from outside. They remember the high-frequency input that got their attention (so to speak) in the first place. Furthermore, the same thing seems to be responsible in forming real-life memories.
Prof. Suzuki’s lecture on LTP is listed as “recommended” in the syllabus. It can be supplemented with this description. You may find that the details are probably better seen in animations here and there. (Click on “narrated”.) Notice that high-frequency (or “tetanic”) stimulation of the hippocampus first depolarizes the dendrite membrane via the AMPA receptors, which then allows the NMDA receptors to open channels for sodium and calcium to enter the cell, resulting in further depolarization and the creation of yet more AMPA receptors in the dendrite membrane. The calcium ions also activate enzymes called kinases that produce other long-term changes using CREB molecules to support memory formation.
Well-informed people are eager to help you understand this process. Here’s Nobel-prize winner Eric Kandel. The BBC ran a three-part series of radio programs that includes this research. (Click on “programme two” and “programme three” in orange for the rest.)
Two Kinds of Amnesia
The basic distinction is between retrograde and anterograde amnesia. A person who has lost the ability to recall events preceding a trauma has retrograde amnesia. Someone who cannot form new permanent memories has anterograde amnesia. It is not uncommon for someone to have both kinds at once.
Retrograde amnesia can occur after a concussion, electric shock, hypothermia, hypoxia, some drugs, an epileptic seizure, or brain damage—almost anything that interrupts the normal operation of the brain for a few moments. Since short-term (or working) memory (STM) exists within the brain as a dynamic pattern of electrical activity, disturbing that pattern—that persisting record of recent experience—makes the memory forever irretrievable. It never had a chance to be consolidated or made permanent in long-term memory (LTM). Therefore the memory of the trauma itself—the car wreck, the near-drowning—is lost forever. In addition to this storage impairment, retrograde amnesia commonly involves some disturbance in recalling already-consolidated memories, too. This is a retrieval impairment, which—unlike the storage failure—often recovers; the earliest memories are always recovered first.
Anterograde amnesia typically occurs with disease or surgery such as Korsakoff’s syndrome, temporal-lobe resection, or Alzheimer’s disease. The patient is left with working memory and, often, an intact LTM, but no way to convert short-term memories to long-term memories—no way to consolidate memories. Such people can hold events in short-term memory for a couple of minutes, if they’re not distracted; they can recall old memories from before the surgery or onset of disease. However, they can’t recall anything recent. They read old magazines anew each day and must be introduced to people each time they meet them. As the book points out, however, they may have lost declarative memories but not implicit memories. They can’t remember your name from yesterday but they may be able to learn a new motor task like mirror writing.
The surgical removal of temporal-lobe tissue caused the most famous case of anterograde amnesia decades ago in H.M., who died in 2008. A disease of thyroid insufficiency sometimes seen in alcoholics, Korsakoff’s syndrome, involves anterograde amnesia. Alcoholics often subsist on poor diets–foods like sugar doughnuts made from refined flour that lacks thiamine. Unfortunately, ethyl alcohol (grain alcohol) blocks the uptake of whatever thiamine (vitamin B1) is left. As a result, alcoholics suffer major thiamine deficiencies. World War II demonstrated that thiamine deficiencies destroy parts of memory. British prisoners of war held by the Japanese were fed polished rice and little else. The rice was not fortified with vitamins. Almost all of the husk, or bran, had been polished off, and that bran was where the rice’s thiamine was concentrated. As a result, the POWs developed beri-beri from thiamine deficiency. They developed heart trouble and memory deficits.
Anatomically, Korsakoff’s syndrome is associated with shrinkage of the hippocampus and with degeneration in several output targets of the hippocampus, such as the mammillary bodies.
Questions (please answer one)
1. At what level(s) of the nervous system are memories formed—molecular, cellular (neuronal), brain systems? Choose one level and describe what happens to form memories or abolish them.
2. Does LTP suggest a process that you might manipulate to prevent or facilitate the formation of memories?
3. How would you distinguish amnesia from normal forgetting? When would you call an absent-minded person amnesic?
4. How might reconsolidation pose a threat of amnesia?
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