The author offered an interesting account of Dr. Harvey who performed the autopsy on Albert Einstein and experimented with his brain. It was discovered that the glia cells, so abundantly present in the human brain can be responsible for the Einstein’s uniqueness. Located in the association cortex, glia cells are unlike the neurons but were found to have a significant affect on the neurons through (first hypothetical) communication between glia cells and neurons.
Through the new findings (Edelman, 1998) it was shown that glia cells influence the formation of synapses that are responsible for the quality of communication between the neurons. Obviously, if the synaptic connections are stronger than the person is capable of more and better associations, learning, and recall.
In addition, another study provides evidence that glia cells establish its own communication network run in parallel to the neuron network. The article confirms that during the time when Einstein lived, neuroscientists believed that glial cells were responsible for the information processing. Although it was agreed that the evidence simply was not there, the work continued and search once again focused on the mysterious function of the presence of glial cells. The author pointed out that the researchers assumed the insignificance due to the inefficiency of equipment to detect the “glial chatter” and the fact that they were looking at glial cells trying to duplicate their search with the same mode as that in neural network.
According to the article, the recent discovery brought the light of this difference: the glial cells communicate chemically not electronically, as it was suspected following the neural model. Brave assertion suggested that the glial cells “listen in” to the neural communication and then react appropriately depending upon what they “hear.” The author also added that according to the earlier work, the influx of calcium cells suggested that the glial cells “had been stimulated.” That assumption was earlier confirmed through and with an imaginative innovation that allowed checking the calcium levels in Schwann cells, the glial cells that surround synapses where neurons meet. The author also wanted to know whether glial cells were limited to what he called “eavesdropping” or had more specialized function, like participating in the direct communication through the neural network. Such hypothesis was later confirms with the described in detail experiment.
The author continued describing his research with the supposition that something else was going on with glial cells. He was not satisfied with the finding that these particular cells were responding to the calcium influx. He used the 1990 study of Stephen J. Smith of Yale University that showed the increase of concentration in calcium in the cells called astrocytes, Such increase was caused when the neurotransmitter glutamate was added to a cell culture and doubled for the natural process during which the neurotransmitter is released by a neuron. Further description of another work by S. Ben Kater in 1996 showed that astrocytes would use extra cellular medium rather physical contact to send impulses. Such conclusion basically displayed the possibility that glial cells could communicate among themselves using the extra cellular medium.
Further research clarified which molecules exactly were involved in glial communication. The author displayed the finding of Peter B. Guthrie in 1999. His finding helped researchers to determine the concrete model of how glial cells reacted to the calcium influx and then communicated to other glial cells by releasing ATP molecules. The only difficulty was to find out how the transmittal would sense the calcium influx for neurotransmitters were not an answer: those would not diffuse out the axon connections. The further experimentation brought the researchers to the realization that ATP molecules were fired out of the axons and picked up by glial cells. Their analysis was a hypothesis that ATP served as the medium of transmission from the neural network to the glial network through the calcium ions. The ions activate enzymes that affect the genes (Selkoe, 2006). The researcher, further down the road, came to the hypothetical (till today) situation which would direct their attention at the genes as controlling agents initiating the above-described mechanism.
At this point, the author described the Steven’s research that explained the function and purpose of myelin insulation around the axons. According to this research, the insulation serves as conducting medium that transmits the nerve impulses “at high speeds over the long distances.” Exactly this work showed the differentiation between axon cells in terms of their development into myelin-surrounded cells or cells with no insulation.
The author continued describing the logistics of the chain in hypotheses by mentioning the work of Vittorio Gallo and his colleagues. The work involved a closer look at oligodendrocyte glia that forms myelin in the brain. According to this work, myelin was produced with the maturation of cells when phosphate molecules in ATP were removed (the substance remained was called adenosine). This conclusion indicated at the differentiation of a neuron to know where to send separate messenger molecules: to central or peripheral nervous systems.
The author connects than with the practical significance of the process behind demyelination explaining that such condition causes debilitating health conditions in too many people. He also mentioned an important finding that although the exact process of myelination is still under research, it is known that adenosine is the first substance that initiates the process. That fact might later lead to discovering treatment to diseases like multiple sclerosis.
Readers later are confronted by an interesting question. Although, the role that ATP and adenosine are known in the myelination process, the researchers are very curious about the possibility of glial cells having the power over regulating the function of neurons (see also (Qiao, Seidler, Tate, Cousins, & Slotkin, 2003). According to the article, Richard Robitaille of the University of Montreal studied the effect of Schwann cells at the synapse on the neurons. It appeared that this particular researcher took a different perspective and instead following the path from neurons to the glial cells he reversed the direction. Another researcher confirmed “waves of calcium sent by glia changed the visual neurons’ in rats. These findings encouraged Maiken Nedergaard of New York Medical College who studied the lesions of rats’ brain taken from the hippocampus, area of the brain responsible for memory. Then it was suggested that glia might play a role in plasticity, the organism’s response through learning.
The author did mention a difficult to understand dilemma: how a large population of calcium influx would be differentiated by and with the entire population of astrocytes. To enact some detailed information processing there should be a mechanism that would detect the specific messengers and differentiate those from the rest. The article of 1990 stated that Smith and his colleagues did believe in the possibility of such differentiation of the mass influx into more discrete packets allowing much more detailed communication. That could not be confirmed for the lack of appropriate equipment. However, Philip G. Haydon of the University of Pennsylvania found (2003) that “there is short-range connectivity between astrocytes.” He used a laser equipment to release a minute quantity of glutamate in the rat’s hippocampal brain region. That quantity was detected by a single astrocyte, which allowed the above conclusion to be made.
The author described then the working hypothesis that consisted of “communication among astrocytes helps to activate neurons whose axons terminate relatively far away and that this activity, in turn, contributes to the release of neurotransmitters at distant synapses. This action would regulate how susceptible remote synapses are to undergoing a change in strength, which is the cellular mechanism underlying learning and memory. “ The article accounted for the work of postdoctoral students, Karen S. Christopherson and Erik M. U1lian who have found the chemical messenger, the protein called thrombospondin, was responsible for the building of synapses. This particular protein was known to play physiological role but was not known to participate within the nervous system. There is a supposition that this protein might bring together proteins and other compounds to help synapse grow.
The author concludes the article by directing the readers’ attention at the possibility of connecting the findings with their possible relationship with the human memory suggesting such interesting idea as, “perhaps a higher concentration of glia, or a more potent type of glia, is what elevates certain humans to genius.” (see also Szpir, 2006) Obviously, there is more to explore.
References
- Edelman, G. M. (1998). Building a Picture of the Brain. Daedalus, 127(2), 37+. Retrieved July 15, 2007
- Qiao, D., Seidler, F. J., Tate, C. A., Cousins, M. M., & Slotkin, T. A. (2003). Fetal Chlorpyrifos Exposure: Adverse Effects on Brain Cell Development and Cholinergic Biomarkers Emerge Postnatally and Continue into Adolescence and Adulthood. Environmental Health Perspectives, 111(4), 536+. Retrieved July 15, 2007, from Questia database: http://www.questia.com/PM.qst?a=o&d=5001931614
- Selkoe, D. J. (2006). The Aging Mind: Deciphering Alzheimer’s Disease & Its Antecedents. Daedalus, 135(1), 58+. Retrieved July 15, 2007, from Questia database: http://www.questia.com/PM.qst?a=o&d=5015009904
- Szpir, M. (2006). New Thinking on Neurodevelopment. Environmental Health Perspectives, 114(2), 100+. Retrieved July 15, 2007, from Questia database: http://www.questia.com/PM.qst?a=o&d=5014162015