Amine-based neurotransmitters

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Posted by Miguel ( on February 11, 2000 at 23:43:30:

In Reply to: Amine neurotransmitter CH connection posted by Bobbie P. on February 11, 2000 at 22:53:54:

Not Bob P here. I found your post interesting in its addressing of the pituitary gland's possible involvement in CH. I started to look into that possiblity after noting some of the aspects posted by Q in his Hypothalamic connection quest. It somehow became evident to me after reading a bit about the hypothalamus funstionality that it is logical to assume that the pituitary gland may also be involved in CH. Some of the connections came from one of my triggers, chocolate. I considered this option a few years ago, but never really followed on it. Also, sex as a trigger, as well as other alkaloids, which may play a role in oxytocin release. In fact, that is why I asked last week or the week before, if pregnancy and nursing produced any changes in CH. As you asked again, and corroborated with other posters, it appears that indeed, CH ceases during pregnancy. Then, there was what may possibly be consider "the clincher" for oxytocin, nursing! It is believed that oxytocin is the primary agent involved in what is known as "milk let down". Oxytocin is a potent smooth muscle agonist. Blood vessels are lined with smooth muscle, so is the uterus, as well as the milk-producing vessicles of the mammary glands in humans. I need to really look into the specifics of this. The only thing that does not quite fit is that I am having difficulty finding data to corroborate headache attacks frequency (if any) and severity subsequent to inducement via i.v. oxytocin.

Questions: Given your data suggesting that males suffering CH experience a lowering of plasma concentration of testosterone:

1) What are the levels of other sex hormones in those males?
2) Women; what happens to estrogen/prgesterone during CH episodes?

I really do not understand the connection between serotonin, LH, pituitary gland-derived secretions.

A mutation of a receptor proding gene, which in turn results in abnormally large receptors. This condition cuasing a decrease in plasma serotonin. I think that is what I understood from your post. Does the paper/manuscript suggest the relationship between the two, larger receptors, lower plasma conc. of serotonin? It would seem that the affinity for a receptor by the corresponding molecule does not change. Such involves chemical afinity relationships, as well as site to moleucle correlative topography. If anything, it seems that it would affect the receptor-molecule interaction adversely, Of course, unless the mutated receptor, with its larger size develops multiple identical receptor site "pockets" for the corresponding molecule. Another alternative would be that a cell membrane-based receptor although large and binding to the same number of molecules, at the same rate of binding and disociation, may in fact have developed several more "pockets" inside the cell, where it is metabolizing, or converting its cell messangers at a faster rate, or from more than the normal amount of internal receptors. Also, it could mean that if an internal cellular meesanger is generated by the receptor, doe it means that more of that messanger is being genrated? This last few "fishing" thoughts of mine, would not justify the decrease in serotonin plasma conc.

You know, at times I think that CH is nothing but a norepi hangover given the stress cycles that I undergo as correlated to my episodic attacks. Other times I think that my baroreceptors are the ones mutated, or acting screwy due to my sensitivity to weather fronts. However, all these go out the window once I landed on this site. The reason is simple - there are too many time frame coincidences for episodic sufferers. This would suggest an external seasonal change that we as sufferes are not able to deal with at the biological level. Of course, it is perhaps due to an internal abnormality, which corroborates some of my thoughts regarding mutations a receptor level, or transmitters, as conveyed to Q during our chat a few days ago. Clearly, chronic CH conditions dispel most of these thought if chronic CH is the same disease as episodic CH, which I am starting to doubt. Migraine and CH were once clumped as one too...

May the beast die a death conmesurate with the life it has given us...


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