The Root of Thought (13 page)

The rule 7 +/– 2 has become a major track in psychological studies. It represents that people can immediately repeat back a series of seven (give or take two) objects in the short term before forgetting them. Psychological research has settled on this number. Also, grouping objects together can add more to the 7 +/– 2 phenomenon. For instance, you can
probably remember the nine letters NTUAGBOSP if you have good short-term memory. However, if you can’t remember nine and have the capability to remember only seven, it would be best to categorize them into groups that you already understand as GUN, PAT, and SOB. This way, you only have to remember three things, which gives you room for four more, so you can remember many more letters.

Memory has been considered since the written language. It was always thought that we possess the ability for short- and long-term memory: one being our constant acknowledgement of our present situation and another being our ability to reach into time and acquire the past.

As the psychological ideas of memory were being categorized with modern scientific terms, the biological seat of memory eluded researches through the nineteenth century and into the twentieth. It was always believed to lie in the cortex after the discoveries set down by French anatomist Pierre Fluorens and later in the work of Germans Gustav Fritz and Eduard Hitzig, which determined that higher thought and information storage occurs in the cortex. Researchers also noticed that our capacity for memory and information storage surpassed other animals (as we understand it) and our cortex is much larger and complex than other animals.

In the 1920s, while looking for a locus of memory in the cortex, Karl Lashley (1890–1958), a psychologist at Harvard, trained rats to run a maze and then removed parts of their cortices. He found that it didn’t matter where he removed parts of the cortex; they learned the same. However, if he removed a substantial amount, they would have trouble. Trying to understand where memory was, he became frustrated and wrote with, tongue in cheek that “reviewing the evidence…learning is just not possible” and “in spite of the evidence against it, learning sometimes does occur.” This ability for information storage to be elusive in the cortex points to the pliable nature of calcium wave communication.

At the same time, Ivan Pavlov (1849–1936) in Russia was showing memory in action with his dog. As everyone with a dog knows, it salivates when presented with food. Pavlov rang a bell every time he gave his dog food and soon the dog salivated only when the bell rung. This type of learning by association held widespread implications for human manipulation and psychologists. This reflexive learning likely resides in the domain of neurons—surpassing astrocyte processing and causing an
unconscious motor reflex. However, to Lashley’s chagrin, this tells us nothing about the seat of memory biologically.

Later, in the 1950s, using the knowledge acquired by Wilder Penfield on the electrical impulses in the brain among awake patients, members of the McGill University staff tried to eliminate epilepsy by removing parts of the brain. They were eventually successful with the removal of tracks of neurons called the corpus callosum that join the right and left hemispheres. However, one of their failures proved to be scientifically useful, if not terrible for the patient. The patient has always been referred to as HM in the scientific literature. They removed the base and part of the sides of his brain, at about the area of the temple and curving under deep into the brain. This area of the brain is called the hippocampus.

The hippocampus is a gateway between the subcoritcal and cortical structures. Hippocampus is Greek for seahorse, and in sections (see
Figure 8.1
), it kind of does look like a seahorse. It curls up like the side of a fist. Inputs come in from basal parts of the brain and go out to the cortex.

FIGURE 8.1 A section through the hippocampus as seen and drawn by Golgi (left) and Cajal (right).

The removal of the hippocampus and the adjacent part of the cortex, referred to as the entorhinal cortex for its similarities to a rhino horn, completely eliminated learning in HM. He was unable to remember anything from one moment to the next. He could not learn beyond a couple minutes before everything he learned was lost. His experience was eerily similar to Alzheimer’s patients without dementia. He was able to recall with long-term memory everything before the surgery, but couldn’t remember anything afterwards because nothing would stick. If information was a light particle, his brain was a black hole.

Oddly, HM could learn and improve from day to day how to draw a picture or play the piano. HM’s physical memory was not impaired. And his intelligence was not affected by losing his hippocampus. He just couldn’t learn any new facts about his existence.

Sherrington, the man who discovered and coined the synapse, first described learning and memory on a cellular level. He confirmed Cajal’s notion that neurons in the brain were separated from each other and referred to the learning and memory in the brain as the enchanted loom, which is like a spinning web of string that can remove, replace, and add new strings at will. He imagined it being spun passively by the workings of our neurons, our environment determining the strength and choice of the strings.

Of course, while studying the Neuron Doctrine in the church of Ramón y Cajal, one can learn that he was the first to propose that synapses become strengthened when learning occurs. This philosophical idea sprung from the knowledge that less synapses could be seen as a person ages. Like many of Cajal’s exquisite ideas, researchers have spent most of the twentieth century until the present ardently attempting to determine its truth.

This idea, combined with Donald Hebb’s notion of “synaptogenesis,” led to two opposing biological tenants regarding learning and memory. These ideas completely disregard the possibility for a role in glia in one of the most important processes in human thought, with wide-ranging implications from intelligence to cures for dementias for the aging.

Donald Hebb’s idea of synapses sprouting extra arms when learning occurs has long been considered true along with Ramón y Cajal’s theory. They have now been combined to indicate that synaptogenesis is how synaptic strength occurs. Eric Kandel and colleagues, using the inert
ocean animal, the aplysia (a type of large sea slug), tested this theory. The aplysia sits on the bottom of the ocean and reacts to incoming stimulus through a series of sensory nerves. Kandel’s experiments were comprehensive and focused strictly on the action of neurons in the simple animal. They found that when stimulating a sensory neuron, the synaptic strength lessened as the animal became habituated.

This analogy can be best understood if one considers the
Blues Brothers
. Jake sees Elwood’s place for the first time since he’s been out of jail. It’s in Chicago right next to the El. Every time the train goes by, the entire apartment rattles as though they are shaken in a box. Jake looks around and asks, “How often does the train go by?” “So often you don’t even notice,” says Elwood.

Elwood’s statement defines habituation. The decrease of transmitter release from neurons as they are repeatedly (habitually) told to fire. If one thinks about this in terms of glia, the excess transmitter release is taken up into the surrounding astrocytes. The astrocytes will then perform calcium waves throughout the area. However, the trigger of becoming habituated might be a signal from the astrocytes back to the neuron to decrease firing.

Another form of learning on the cellular level described by Kandel is called sensitization; this is the result of combining a normal stimulus with a noxious stimulus, creating a stronger synapse. For instance, if as you are reading this and you get kicked in the shins out of the blue, you might get sick to your stomach the next time you read this paragraph.

Learning through sensitization in humans can also be regarded when one thinks of the instant of Kennedy being shot, the Challenger disaster, or the terrorist attacks in 2001. People distinctly remember where they were when these events occurred. The increase in synaptic strength from sensitization is also the result of increased neurotransmitter release.

Glial function during the phenomenon of habituation and sensitization has not been studied. Synaptogenesis, as described by Hebb, is glial dependent. Increased or lack of transmitter at the synapse could also be the result of glial function. After the glial process the excess transmitter (the sensory input from getting “kicked in the shins”), the glia will not allow the neurons to become habituated. Instead, the glial cells let the nerouns continue to fire extreme amounts of transmitters in the advent it
might happen again and you will be reflexively prepared. All associated stimulus will also be primed. The glial cell centers know processing is not needed and open the neuronal floodgates.

However, studies spearheaded by the work of Joseph Altman in the late 1960s at Purdue University started a new line of research pertaining to memory in the area of ”adult neurogenesis.” In relation to learning, Cajal firmly believed that after development, cell growth is halted, and the brain remains in its state until we die. His notion of increased synaptic strength fit into his neuronal dominated theory for thought and gave room for the possibility of slight changes to incorporate the obvious phenomenon of learning and memory.

Altman’s idea abolished one of the facts most researchers took for granted without examining closely. Obviously, his studies met with staunch resistance. His experiments were completely overlooked. No one wanted to consider an experiment that claimed new cells divided in adult rats, much less that learning could increase cell division.

Altman took rats and had them perform learning tasks while injecting them with radioactive thymidine. Thymidine can insert itself into the DNA of cells in the process of dividing. When the brain is removed and sliced up, then stained for thymidine, the researcher can see where the cells were dividing. After periods of intense learning, Altman discovered cell division in the hippocampus increases and that some of these cells form neurons.

Now it is known that the cells that initially divide through adulthood in the hippocampus are astrocytes.

Altman’s studies were buried by the discovery of long-term potentiation (LTP) in 1973 by Tim Bliss and Terje Lømo in England. LTP is the fancy way of saying synaptic strength increase shown electrically. They took out the hippocampus of rats after they performed maze learning. They were able to determine electrophysiologically that neurons required fewer stimuli to fire in the hippocampus of rats that had learned. Through learning, the neurons had been primed and sensitized. Thee threshold had been lowered for the firing to occur, as if one could barely breathe on a gun trigger to get it to fire.

LTP is still being worked on extensively, but the idea is simply an electrical confirmation of the synaptic strength theory proposed by Cajal, Sherrington, and Hebb, and confirmed molecularly by Kandel. The notion of LTP receiving so much attention is similar to if someone saying
a wheel is round made front-page news. LTP has yet to be confirmed in humans.

Altman’s studies were forgotten for 20 years until Arturo Alvarez-Buylla and Fernando Nottebohm ignited the field by confirming cellular genesis in adult songbirds learning new songs. Now we know that humans also regenerate new cells throughout their life and all newly regenerating cells in adults are astrocytes. Alvarez-Buylla and colleagues have shown conclusively that the regenerating cell is not a neuron. They have characteristics of astrocytes, turning over to produce more astrocytes and only occasionally producing a neuron. The implication that astrocytes are the seat of information through cell growth during learning and memory processes is just gaining steam.

Astrocytes constantly divide in our brain throughout adulthood. When we learn, they divide more rapidly. In the hippocampus, they occasionally become neurons. Similar to when a city grows to the outskirts and the town commission decides to build a new highway, astrocytes decide to lay down a new neuron.

In the 1990s, Fred Gage and colleagues at the Salk Institute in San Diego confirmed that cell division occurs in the human hippocampus; other labs have shown that the cells dividing in humans are astrocytes.

When discussing thought, it must be noted that learning is not intelligence; education improves intelligence as judged by standardized tests, but most would agree that intelligence is not education-dependent. Someone who only made it through the third grade can think on a higher level than someone with a graduate degree. It’s a matter of using your brain and learning many things to draw from, whether it is facts about human anatomy or nuances of human body language. Astrocyte cell growth is essential to this process.

The nature of the glia communicatory fashion indicates that they might contribute to memory in the cortex. Hebb suggested that assemblies of cells, distributed over large areas of cortex, work together to represent information. This idea, which Hebb believed occurred with neurons, can now be explained as the domain of glia. A glial center can access neurons to travel long distances, and astrocytes control all compartments of the cortex. The only way to abolish cortical memory is to block glutamate reuptake—a function that is dominated by astrocytes.