[paula_w]

There are many neurotransmitters but the ones we keep hearing and reading about are dopamine, acetylcholine, norepinepherine, glutamate/gaba, and serotonin.

By the way and I don't say this to be snide. i was researching hormones and it led to sex hormones which of course affects me because i had young onset menopause and other hormonal precursors to motor problems. knowing that if this path would eliminate men i read some about male sex hormones. it was fulll of what each transmitter does to produce a fertile sperm...neurotransmitters that is.

i accidentally hit enter so will continue on the next post.

[paula_w]

http://en.wikipedia.org/wiki/Somatic_nervous_system
Somatic nervous system
part of the peripheral nervous system and responsible for skeletal muscles. It is always an excitatory transmision in vertabrates. Governs voluntary movements of skeletal muscles.

acetycholine (Ach) is the only neurotransmitter in this system.

an opinion:
IMHO acetylcholine is involved with dystonia, tremor and possible dyskinesia if you have too much of it. chances are, the more advanced you get, you will not replenish dopamine as you sleep, and theoretically could wake up with dystonia from having normal to above normal acetylcholine and low dopamine. and norepinephrine.

i'm taking Pamelor, nortriptyline, whose function increases norepinepherine,which is another transmitter typically low in Parkinson disease; it also acts to break down acetylcholine , making it an anticholinergic substance too, Since i began taking it, my morning dystonia is greatly diminished. sometimes i don't get it at all. Just pd isn't as bad as pd with dystonia.

this bares witness to my belief that too much acetylcholine will cause muscle cramping when off, and can cause peripheral weakness to the point of paralysis even when on. It is toxic and used in chemical warfare. There is a hereditary condition called pseudo cholinesterase deficiency, in which a person born with it won't ever know unless they have surgery and a certain substance is in the anesthesia. This condition robs you of the enzyme that breaks down acetylcholine and causes it to build up in your system. Then if on top of that , a chemical containing more of the same is used in anesthesia with this condition will cause even the heart to become paralyzed and patients have to be resuscitated. It causes death in children.

On the other side of the acetycholine fence, is the fact that they think it is what alzheimers patients are lacking and that line of drugs boosts more acetylcholine. They don't work long if at all ( a couple months?) and pwp do not need it for their cognitive problems unless they have alzheimers type dementia. The line is called cholinergic inhibitors and it blocks the enzyme transmission to break acetylcholine down.

IF a person has too much acetylcholine (already out of balance in parkinson s with the other neurotransmitters like dopamine and norepinephrine) is given a cholinesterase inhibitor [alzheimers med ] the result could be serious - paralysis and extreme peripheral weakess was the result when my neuro thought i could try aricept for pwp cognitive problems. people without any acetycholine deficiency do not need to inhibit it's breakdown and build up even more.

i'm going to take a break and post this before i lose it. anyone is free to jump in. i have alot more.


http://en.wikipedia.org/wiki/Enteric_nervous_system

[paula_w]

http://en.wikipedia.org/wiki/Enteric_nervous_system
Enteric system
a subdivision of the peripheral nervous system (PNS), that directly controls the gastrointestinal system

The enteric nervous system also makes use of more than 30 neurotransmitters, most of which are identical to the ones found in CNS, such as acetylcholine, dopamine, and serotonin. The enteric nervous system has the capacity to alter its response depending on such factors as bulk and nutrient composition. In addition, ENS contains support cells which are similar to astroglia of the brain and a diffusion barrier around the capillaries surrounding ganglia which is similar to the blood-brain barrier of cerebral blood vessels.[10]

The enteric nervous system has been described as a "second brain".[9] There are several reasons for this. The enteric nervous system can operate autonomously. It normally communicates with the CNS through the parasympathetic (eg, via the vagus nerve) and sympathetic (eg, via the prevertebral ganglia) nervous systems. However, vertebrate studies show that when the vagus nerve is severed, the enteric nervous system continues to function.

http://en.wikipedia.org/wiki/Enteric...stem#Function\

Enteric neurons secrete an intimidating array of neurotransmitters. One major neurotransmitter produced by enteric neurons is acetylcholine. In general, neurons that secrete acetylcholine are excitatory, stimulating smooth muscle contraction, increases in intestinal secretions, release of enteric hormones and dilation of blood vessels. Norepinephrine is also used extensively for neurotransmission in the gastrointestinal tract, but it derives from extrinsic sympathetic neurons; the effect of norepinephrine is almost always inhibitory and opposite that of acetylcholine.

http://www.vivo.colostate.edu/hbooks...i_nervous.html

opinion; so we have low norepinephrine and definite imbalance in our gastrointestinal system.....diarrhea, constipation, irritable bowel syndrome is a neurotransmitter imbalance in part. it's just partly opinion, I think i read that it is indeed that but i don't remember where.

[reverett123]

http://www.brainexplorer.org/neurolo...smitters.shtml

Almost easy to understand.

[paula_w]

Here's where I kinda stopped, with more on gaba, serotonin coming, and others as they learn more. I'm starting to get it. Everything has an effect and if the enteric " brain' is automatic [i know it was called a more medical term] mine should be doing more!

They are half brained in research don't u think? I don't know of much research about the " other Brain" and know it's an old concept. It seems very important.

More later or tomorrow. Would love you to add or comment

thanks

[paula_w]

http://www.springerlink.com/content/kdbt7gh6q2dua0xf/

there are two or 3 articles so scroll down

adding
thanks - the site is really substantial and concise.

[paula_w]

http://www.sciencedaily.com/releases...0813171117.htm

Loss Of Two Types Of Neurons Triggers Parkinson's Symptoms, Study Suggests

ScienceDaily (Aug. 14, 2007) — New evidence indicates that the loss of two types of brain cells--not just one as previously thought--may trigger the onset of symptoms associated with Parkinson's disease.


The evidence, based on mouse models, shows a link between the loss of both norepinephrine and dopamine neurons and the delayed onset of symptoms associated with Parkinson's disease. It was originally thought that the loss of only dopamine neurons triggered symptoms.....

....The dogma in the field is that Parkinson's disease involves a selective loss of dopamine neurons. The truth is, if you look at postmortem Parkinson's disease brains, you will see that both dopamine and norepinephrine neurons are gone," Dr. Weinshenker explains

http://www.sciencedaily.com/releases...0813171117.htm


http://www.michaeljfox.org/newsEvent...cle.cfm?ID=231

Weinshenker adds that in terms of therapies for Parkinson's patients, "it might be worth treating the norepinephrine as well as the dopamine system," by supplementing the drug L-dopa, the current standard in care, with a tricyclic antidepressant, which is known to improve norepinephrine signaling."

[paula_w]

http://www.benbest.com/science/anatm...html#glutamate

This is the most complicated transmitter and always excitatory. I defer to the links for more explanation. The link below, however, demonstrates progress in its therapeutic potential and is a pretty important discovery.

Glutamate is considered to be a critical transmitter that has abnormal signaling in parkinson's and other movement circuit conditions.


http://www.dddmag.com/article-Glutam...py-101310.aspx

This one is in therapeutic experimentation. From the article a most promising find:

ADX48621, an mGluR5 NAM being developed by Addex Pharmaceuticals has shown efficacy in a non-human primate model of PD-LID.5

These data suggest that ADX48621 is differentiated and shows considerable efficacy on both components of dyskinesia–chorea and dystonia.

Indeed, we believe ADX48621 is the first and only product to have been reported to have efficacy on dystonia in this model of PD-LID.

ADX48621 has completed Phase 1 testing and is initiating one study for ADX48621 in PD-LID patients and a second study for ADX48621 in patients with dystonia.

[pd-lid] = pd levodopa induced dystonia.

[paula_w]

Bulletin of Experimental Biology and Medicine
Volume 145, Number 5, 584-587, DOI: 10.1007/s10517-008-0141-3


Autoantibodies against glutamate, γ-aminobutyric acid, and norepinephrine in mechanisms of neuropathic pain syndrome

V. A. Evseev, L. A. Vetrile, V. S. Smirnova, V. N. Grafova, I. A. Zaharova, N. A. Trekova and M. L. Kukushkin

Glutamate


The production and role of autoantibodies against neurotransmitters glutamate, γ-aminobutyric acid, and norepinephrine were studied in rats with experimental neuropathic pain syndrome induced by sciatic nerve transection. The development of neuropathic pain syndrome was accompanied by increased production of autoantibodies against glutamate, γ-aminobutyric acid, and norepinephrine. Our results suggest that antibodies against glutamate and norepinephrine exhibit protective activity.

http://www.springerlink.com/content/b5t7431760001191/

[paula_w]

http://neuromuscular.wustl.edu/mother/acetylcholine.htm

it's pretty bad, when you get excited finding a site like this..below lol

http://neuromuscular.wustl.edu/synmg.html

http://neuromuscular.wustl.edu/syaltbrain.html

it goes on and on...you could pass through it and come out an MD..

tossing out another one

http://neuromuscular.wustl.edu/msys/mend.htm