Teach the Brain Forums

OECD expert Wrote:This issue of teacher training is a central one. What sort of neurobiological knowledge do you believe would be appropriate to incorporate into a teacher training program?

Thanks very much for your insights and input,
Christina

This is a very good question and one I have been thinking about for some time. This is one of the questions that I am going to ask Larry Squire when we have lunch on the 15th of September. I know that we will not necessarily agree because of the molecular background that he has, however you never know. I am a little reticent to outline my ideas as this point but cell biology would be very important. Also as Marian Diamond has mentioned a number of times that...we really do need basic anatomy and physiology. I am not too knowledgeable about Kandel's proposal or idea or "what have you" for teaching a new synthesis...the molecular biology of cognition.

I am truly speaking of what prior knowledge in the area of neurobiology does a teacher need inorder to understand fully the area of the functions of the brain and both the CNS and PNS. I have a feeling that my job at present of being course custodian [Discover Learning In the Mind, Brain and Body]of all 30 Chapman University Colleges in California and the State of Washington will be defined this next term with my introduction of a text similar to Memory:From mind to molecules by Larry Squire and Eric Kandel as a mandated text. In the mean time....we must determine how deep into the sciences we need to go. I just keep going and going and going like that battery advertisement. That is obsessive, but I know it.

I guess that I don't have a specific answer for you, but I am going to begin forthwith into the neurobiology as a text mandate along with discussing this with Kurt Fischer. My website has the syllabus for Discover learning in the mind, brain and body. This is being revised [by me]to cover less theory and cover more indepth neurobiology. The assessments will be really creative...and most likely open to the public. You are welcome to look at this program that I will revise since I wrote it.....there should not be too many tears [Everthough a great deal of work]. My website is located under my personal profile here on Teach-the -Brain Forums.

Be well,
Rob

Thanks very much for this Rob. It sounds like you have put quite a lot of thought into this already.

Do others have input/opinions on this subject?

Best,
Christina

We know that the neuron communicates within the boundaries of itself...the neuron. We know that the neuron communicates with other neurons outside itself. However to communicate with other neurons it will need to have the ability to communicate via the synapse between the neuron terminal or presynaptic terminal and the target neuron on the other side of the synaptic cleft or gap [if you will] to a receptor of the receiving post synaptic neuron[usually a receptor on the dendrite. This of course is realized by transduction and is absolutely critical for communications. Yet this is an area where things could go wrong and disease or deficit functioning could be delayed or cease.

Now a great deal of research is highlighting the supporting cell of the neuron [the glial cell or glia] The glial cell maintains a presence in the brain that is said to be 10 or 20 or more time the number of neuron cells. They have been noted for being the salient support cell for the neuron. We now are finding out that the glial cell does communicate with other glial cells and this is just the beginning of the research that could lead us to a cure for pediatric glianoma and other such horrible tumors and diseases. Our decade of the brain has proven without any question that we can do research and we can solve problems if the environmental structures are kept funded and people respect life. Glia cells are communicating with neurons? Well we shall soon see.
Best,
Rob

Yes indeed....Neurons deserve lots of study....
URL retrieve September 16, 2005;
Be well,
Rob URL: http://www1.lf1.cuni.cz/~zfisar/bpen/neurobiology.htm

Hi, A Synapse In The Brain Is Really Importan

Since the neuron theory evinces that each neuron be separated by each and every other neuron by a synapse or space between each neuron, we must question the degree of communication deficits that can happen and do happen to adults and children right at the area surrounding the synapse. One of the very earliest synaptic disease is called myasthenia gravis (where nerves stimulate nerve plates).

I aways thought that Parkinson's disease was due to so many dopaminergic nerves that died in the substantia nigra...well actually I am right but Parkinson's is also being referred to as a synaptic disease. Rapport, M.D., R. Nerve Endings: The discovery of the synapse: The quest to find how brain cells communicate [2005] Pg. 199.

...and now that we think clearly about the synapse and that is present throughout the body...it is truly remarkable that we have so few communication disorders. But that is not true either, we have many communcation disorders labeled under a myriad of other diseases. The synapse is very special and will need to be studied in greater depth.
Be well,
Rob

No neurons; no life...is it that simple or drastic? Yes, we can hang on for a time being, but eventually without learning, communications and memory along with progressive brain disease, it becomes very difficult for all. Generally speaking when a neurologist is dxing for a degenerative brain disease or in this example Parkinson's disease...it is most difficult to evaluate since there must be a substantial number of dead or dying dopaminergic neurons in the substantia nigra...which are manifested in the patients slow walking and many other symtoms. Many time with Parkinson's Disease, there cannot be a clear clinical dx...until 70-80% of the neurons have died (dopaminergic neurons).

But you know, symtoms can be treated with dopamine agonists to possible delay as long as possible total degeneration....the dopamine agonist does not cross the blood brain barrier and as time goes on....you need to increase the amount of dopamine agonists that you take by mouth. However, L-dopa does treat the symtoms also and it does cross the blood brain barrier...., but you usually wait to use L-dopa since the symptomatic effect of dopamine agonist wear off. Then you address L-dopa and it works very well in most cases. The L-dopa in time also reaches a point that it cannot be as effective. (Reaches tolerance level and wears off)...but again with this disease, the research with new medications is doing its very best to benefit a better quality longer life. The structural implant is another tool that is working in a number of cases...so progress for a longer life with increasing quality is better. I believe this is the decade to find a cure for Parkinson's disease.

See how important neurons are in maintaining life and communicating....There are many different kinds of neurons and some of these problems will be solved with nondifferentiated stem cells.
Best,
Rob

Remember what happens when the myelin degenerates from the axon of the neuron....well it slows down and stops communications from one neuron to another....via the synapse of course. One demyelinating disease that we are familar with is MS.
Glial cells help support the neurons and help in the remyelination of axon....until they are destroyed by disease....I think that we will cure this within the decade.
Be well,
Rob

segarama Wrote: Remember what happens when the myelin degenerates from the axon of the neuron....well it slows down and stops communications from one neuron to another....via the synapse of course. One demyelinating disease that we are familar with is MS.
Glial cells help support the neurons and help in the remyelination of axon....until they are destroyed by disease....I think that we will cure this within the decade.
Be well,
Rob

Hi Rob,
In regard to your mention of De-myelination, you wrote that it slows and stops communicating?
Though Myelin is equivalent to the plastic coating on an electrical cable.
Where the loss of the coating, causes a short-circuit. Or rather a loss of directional flow.
I would add that Myelin is formed from VLCFA's- very long chain fatty acids.
Yet Myelin is built from the EPA and DHA forms of VLCFA's.
Though it can convert the ALA form into these, though it's not an efficient process.
Of note, is some research into Addison's Disease, which has identified that 'saturated' VLCFA's cause a sort of blockage in their disposal, in the ongoing rebuilding process. Where their elimination and replacement with the 'Unsaturated' forms have been shown to have a remedial effect.
Given that Myelin constitutes the larger part of our Brain.
The brain is mainly a 'lump of fat', with some Grey Cells in the mix.
Though the type and quality of the VLCFA's in our diet, has been shown to directly effect its functionality.

Also in your previous message, you wrote: "No neurons; no life ... ."
Where I know of some Politicians who might be a contradiction of this theory?
Perhaps you've come across some of this species yourself?
Geoff.

Hi Geoff, I retrieved an interesting Url from the internet 10-3-05 regarding myelin and fatty acids et al. in the brain...enjoy....
Be well, URL:http://www.fi.edu/brain/fats.htm
Rob

If what I have been reading about mirror neurons is true, we may have some exciting new underpinnings for learning. Retrieve from internet Nov. 11, 2005.
URL:http://www.pbs.org/wgbh/nova/sciencenow/...4/i01.html
Best,
Rob

Hi, Well we have been living with the neuron doctrine for over a hundred years....you will find some very interesting things; website: http://www.scienceweek.com

Best,
Rob

Hi, If we are going to know a great deal about the neuron and communications then we must know about the CNS and PNS...I retrieved a url November 27,2005 from the internet that is a good read.
URL: http://scienceweek.com/2005/sw051202-6.htm

Best,
Rob

Hi

Good article on mirror neurons and autism retrieved December 5, 2005.
URL: http://sidesearch.lycos.com/?query=UCLA+...ault%2Ehtm


Best,
Rob

Hi

Excellent url retrieved 12-09-05 on the internet.
URL: http://www.learner.org/channel/courses/b...uro_2.html
Be well,
Rob

Hi,
Retrieved 12-9-05 from the internet.
URL: ScienceWeek
Be well, Rob
NEUROBIOLOGY: TRIGGERS AND THE OPENING OF ION CHANNELS

The following points are made by Cynthia Czajkowski (Nature 2005 438:167):

1) Chemical signalling in the brain involves the rapid opening and closing of channels known as ligand-gated ion channels, which lie in the membranes of nerve cells. Binding of a specific activator (a ligand) to these proteins triggers the opening of an integral pore through the membrane in as little as tens of microseconds[1]. Although we know a fair amount about the structure of ligand-gated ion channels, the mechanisms by which the binding of a ligand triggers channel opening are still under debate. New work[2] identifies a network of interacting amino-acid residues in one such protein, and reveals a pathway by which changes at the protein's ligand-binding site can be propagated to its channel region. Further new work[3] identifies a proline residue that acts as a molecular switch to control channel opening. Together, the two reports provide a compelling description of the structural machinery that couples ligand binding to channel gating.

2) Communication between nerve cells takes place at junctions called synapses. When a presynaptic cell is activated, it releases neurochemicals (neurotransmitters) across the synapse that bind to ligand-gated ion channels on the surface of the postsynaptic cell. Binding of neurotransmitter causes the channels to open, allowing ions to flood across the postsynaptic-cell membrane and change the cell's activity. So ligand-gated ion channels can be thought of as transducers that rapidly convert chemical signals into an electrical output. Their opening and closing regulate information flow throughout the brain, and mutations in these channels are responsible for a number of "channelopathies", such as congenital myasthenic syndromes, epileptic disorders, and hereditary hyperekplexia.

3) Lee and Sine[2] and Lummis et al[3] examined the structures of two members of the "Cys-loop" family of ligand-gated ion channels. This family includes channels that respond to the neurotransmitters acetylcholine, serotonin, gamma-aminobutyric acid (GABA), and glycine. The receptors are large transmembrane proteins (molecular weight 300,000) consisting of five similar subunits arranged around a central ion-conducting channel, with each subunit contributing to the lining of the transmembrane channel. The neurotransmitter binds to the extracellular interface between two subunits. But what has long puzzled researchers is how the binding of a neurotransmitter, which is around 6 angstroms long, is translated so rapidly into the opening of an ion channel more than 50 angstroms away in the transmembrane domain of the receptor.

4) Lee and Sine[2] set out to answer this question. They used the nicotinic acetylcholine receptor, whose structure was recently refined to 4-angstrom resolution[4], to identify receptor amino acids that could physically link the binding site to the channel. They then created a series of mutations, by substituting amino acids, to break these potential links, and analyzed the mutations' effects, both individually and in combinations, on channel activity. As a result, they identified a set of interacting residues that functionally and structurally link the binding site to the channel.

References (abridged):

1. Chakrapani, S. & Auerbach, A. Proc. Natl Acad. Sci. USA 102, 87-92 (2004)

2. Lee, W. Y. & Sine, S. M. Nature 438, 243-247 (2005)

3. Lummis, S. C. R. et al. Nature 438, 248-252 (2005)

4. Unwin, N. J. Mol. Biol. 346, 967-989 (2005)

5. Hu, X. Q., Zhang, L., Stewart, R. R. & Weight, R. R. Nature 421, 272-275 (2003)

Nature http://www.nature.com/nature

--------------------------------

segarama Wrote: Hi,
Retrieved 12-9-05 from the internet.
URL: ScienceWeek
Be well, Rob
NEUROBIOLOGY: TRIGGERS AND THE OPENING OF ION CHANNELS

The following points are made by Cynthia Czajkowski (Nature 2005 438:167):

1) Chemical signalling in the brain involves the rapid opening and closing of channels known as ligand-gated ion channels, which lie in the membranes of nerve cells. Binding of a specific activator (a ligand) to these proteins triggers the opening of an integral pore through the membrane in as little as tens of microseconds[1]. Although we know a fair amount about the structure of ligand-gated ion channels, the mechanisms by which the binding of a ligand triggers channel opening are still under debate. New work[2] identifies a network of interacting amino-acid residues in one such protein, and reveals a pathway by which changes at the protein's ligand-binding site can be propagated to its channel region. Further new work[3] identifies a proline residue that acts as a molecular switch to control channel opening. Together, the two reports provide a compelling description of the structural machinery that couples ligand binding to channel gating.

2) Communication between nerve cells takes place at junctions called synapses. When a presynaptic cell is activated, it releases neurochemicals (neurotransmitters) across the synapse that bind to ligand-gated ion channels on the surface of the postsynaptic cell. Binding of neurotransmitter causes the channels to open, allowing ions to flood across the postsynaptic-cell membrane and change the cell's activity. So ligand-gated ion channels can be thought of as transducers that rapidly convert chemical signals into an electrical output. Their opening and closing regulate information flow throughout the brain, and mutations in these channels are responsible for a number of "channelopathies", such as congenital myasthenic syndromes, epileptic disorders, and hereditary hyperekplexia.

3) Lee and Sine[2] and Lummis et al[3] examined the structures of two members of the "Cys-loop" family of ligand-gated ion channels. This family includes channels that respond to the neurotransmitters acetylcholine, serotonin, gamma-aminobutyric acid (GABA), and glycine. The receptors are large transmembrane proteins (molecular weight 300,000) consisting of five similar subunits arranged around a central ion-conducting channel, with each subunit contributing to the lining of the transmembrane channel. The neurotransmitter binds to the extracellular interface between two subunits. But what has long puzzled researchers is how the binding of a neurotransmitter, which is around 6 angstroms long, is translated so rapidly into the opening of an ion channel more than 50 angstroms away in the transmembrane domain of the receptor.

4) Lee and Sine[2] set out to answer this question. They used the nicotinic acetylcholine receptor, whose structure was recently refined to 4-angstrom resolution[4], to identify receptor amino acids that could physically link the binding site to the channel. They then created a series of mutations, by substituting amino acids, to break these potential links, and analyzed the mutations' effects, both individually and in combinations, on channel activity. As a result, they identified a set of interacting residues that functionally and structurally link the binding site to the channel.

References (abridged):

1. Chakrapani, S. & Auerbach, A. Proc. Natl Acad. Sci. USA 102, 87-92 (2004)

2. Lee, W. Y. & Sine, S. M. Nature 438, 243-247 (2005)

3. Lummis, S. C. R. et al. Nature 438, 248-252 (2005)

4. Unwin, N. J. Mol. Biol. 346, 967-989 (2005)

5. Hu, X. Q., Zhang, L., Stewart, R. R. & Weight, R. R. Nature 421, 272-275 (2003)

Nature http://www.nature.com/nature

--------------------------------

Hi I retrieved a very excellent URL from the internet that really explains the neurons and et al. very well. December 14, 2005.
Best,
Rob URL: http://www.learner.org/channel/courses/b...uro_2.html

Please be sure that when you get to the end of the first hyperlink page....click the word 'next' and you will continue on from page to page...[good material]

Hi ..Retrieved from the internet 12-15-05.
Best,
Rob
How Stem Cells Become Brain Cells, OHSU Discovery
15 Dec 2005

Researchers at the Oregon National Primate Research Center at Oregon Health & Science University (OHSU) have discovered one key gene that appears to control how stem cells become various kinds of brain cells. The finding has significant implications for the study of Parkinson's disease, brain and spinal cord injury, and other conditions or diseases that might be combated by replacing lost or damaged brain cells. The research is published in the current online edition of the medical journal Developmental Biology.

"In the early stages of brain development prior to birth, brain stem cells, also known as neural stem cells, will differentiate into neurons," explained Larry Sherman, Ph.D., an associate scientist in the Division of Neuroscience at the Oregon National Primate Research Center and an adjunct associate professor of cell and developmental biology in the OHSU School of Medicine. "In later stages, these same stem cells suddenly start becoming glial cells, which perform a number of functions that include supporting the neurons. We wanted to find out what factors cause this switch in differentiation. We also wanted to determine if the process can be controlled and used as a possible therapy. What amazed us is that it turns out a single gene may be responsible for this incredibly important task."

The key gene that the scientists studied is called brahma-related gene-1 (Brg-1) that is found in both mice and humans. This protein had been previously studied extensively in human cancers, but not in the nervous system. To determine the precise role of Brg-1, Sherman, in collaboration with Dr. Steven Matsumoto from the Integrative Biosciences Department at the OHSU School of Dentistry, bred mice lacking the gene in the nervous system. This resulted in the development of embryos with smaller brains containing neurons but virtually no glial cells. When they isolated neural stem cells, placed them into cell culture and then removed Brg1, the cells in the culture turned into neurons but failed to differentiate into glia.

"This research shows us that in mice, Brg-1 is a critical signal that prevents stem cells from turning into neurons at the wrong time. However, since we can manipulate Brg1 expression in stem cells in culture, we now have a powerful way to generate neurons that could be used to replace cells lost in a variety of diseases and conditions that affect the brain and spinal cord. That is our next step." said Sherman. "Since the process only involves a single gene, it is highly amenable for the development of drugs targeted at promoting stem cell differentiation in the adult nervous system."

While much more research needs to be conducted, the scientists believe these findings could play a role in the development of therapies to combat a variety of diseases and conditions. For instance, Parkinson's disease is related to the loss of dopamine-producing brain cells. Scientists hypothesize that it may be possible to correctly time the expression of brg-1 in neuronal stem cells either in a culture dish or in the brain to replace the lost dopamine-producing cells. Another possibility would be the replacement of lost or damaged motor neurons in patients who have suffered brain or spinal cord damage.

This research was funded in part by the Medical Research Foundation of Oregon, the National Institute's of Health and the Christopher Reeve Paralysis Foundation.

"CRF is pleased to have provided support for this study", said Susan Howley, Director of Research and Executive Vice President, Christopher Reeve Foundation. "Identifying a gene that controls how stem cells turn into different kinds of nerve cells has important implications for clinical application in spinal cord repair strategies."

The ONPRC is a registered research institution, inspected regularly by the United States Department of Agriculture. It operates in compliance with the Animal Welfare Act and has an assurance of regulatory compliance on file with the National Institutes of Health. The ONPRC also participates in the voluntary accreditation program overseen by the Association for Assessment and Accreditation of Laboratory Animal Care International.

Jim Newman
newmanj@ohsu.edu
Oregon Health & Science University
http://www.ohsu.edu

Good morning , What is a giant neuron? Is it just a neuron that is very large? Anything in particular that differentiates the Neuron Theory from the Giant Neuron....Retrieved URL from internet 12-18-05.
URL: http://uk.ask.com/fr?u=http%3A%2F%2Ffacu...amples&mb=

URL: http://uk.ask.com/fr?u=http%3A%2F%2Fweba...20400x&mb=
Be well,
Rob

Hi Rob,

Thanks for this.

A giant neuron is a neuron in an invertebrate with an exceptionally large axon diameter. It is often over ten times larger than other axons in the nervous system!

All the best,
Christina

OECD expert Wrote:Hi Rob,

Thanks for this.

A giant neuron is a neuron in an invertebrate with an exceptionally large axon diameter. It is often over ten times larger than other axons in the nervous system!

All the best,
Christina

Christina,
What is the purpose of the giant neuron?
Rob

Rob,
I think I read that it enables a greater number of direct dendrite connections.
Geoff.

January 10, 2006

I found some urls online 1-10-06 Giant neurons [invertebrates]....interesting read.
Be well,
Rob URL: http://scholar.google.com/scholar?q=Gian...tnG=Search
URL: [url]http://www3.interscience.wiley.com/cgi-bin/abstract/109692269/ABSTRACT?CRETRY=1&SRETRY=0
[/url]
URL: http://www3.interscience.wiley.com/cgi-b...7/ABSTRACT

Hi
The neuron theory really makes the neuron a separate functioning nerve cell....according to the theory, the neuron is not attached to other neurons and communications is such that a synapse is situated between every neuron in the body...the neurons do not physically touch each other but perforce by way of the synapse [ action potential] and the neurotransmitters that release chemicals down the synaptic gap...which targets a receiving neuron on the other side of the synapse...[usually a dendrite]. There is more to it than this simple explanation but the point is that the neuron does not have a direct line of communication continually through other neurons as if it were one long continuous nerve cell...and things do go wrong health wise to the cells, the synapses etc.
Be well, URL: retrieved Jan. 30, 2006 from the
Rob
internet.....http://www.biologymad.com/NervousSystem/synapses.htm

February 3, 2006

Good Evening,

Do we really know how neurons communicate? Do we really know to whom the neurons communicate?
As we know the Neuron Theory states that the neurons are not a continuous long line of nerve cells, but indeed each neuron is separated by a synapse. This is where the neurotransmitted make some good sense. Do we really know what a neurotransmitter does.....Please look over this particular url retrieved 2-03-06 from the internet regarding neurotransmitters and their function.
URL: http://faculty.washington.edu/chudler/chnt1.html
Rob

March 2, 2006

Good day,

If you take a good look at the functions of the brain, you will note that the neurons and the synapses play a really major role in our brain system. Practitioners really need to know a great deal about neurons and synapses....Please trust your judgement and use the internet and see why they are so important. ...or scroll back in this thread and you will be refreshed as to their importance.
Best,
Rob