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Topic: 5HT receptors... study (Read 349 times) |
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dougW
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5HT receptors... study
« on: May 30th, 2003, 8:26am » |
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another article in Cephalalgia, Volume 23 Issue 5 Page 354 - June 2003. Studies before have shown messed up 5HT processes, now another.
I can't get the full article (yet).
Doug Wright
Abnormal 5-HT1D receptor function in cluster headache: a neuroendocrine study with sumatriptan
L Pinessi, I Rainero, W Valfrč, R Lo Giudice, M Ferrero, C Rivoiro, E Arvat1, L Gianotti1, P Del Rizzo2 & P Limone2
The purpose of this study was to assess the sensitivity of 5-HT1D receptors in patients with episodic cluster headache using sumatriptan as a pharmacological probe. The drug, a selective 5-HT1B/1D agonist, stimulates the secretion of growth hormone and inhibits the release of prolactin, adrenocorticotropic hormone (ACTH) and cortisol. These effects may be used to explore the function of serotonergic systems in vivo. We administered subcutaneous sumatriptan and placebo to 20 patients with cluster headache (10 in the active phase and 10 in the remission period) and to 12 controls. The sumatriptan-induced increase of growth hormone concentrations was significantly (P < 0.05) blunted in patients with active cluster headache. Prolactin and ACTH responses to the drug were significantly (P < 0.05) reduced in patients with cluster headache, both in the active and in the remission period. Our results suggest that cerebral serotonergic functions mediated by 5-HT1D receptors are altered in patients with episodic cluster headache.
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CJohnson
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Re: 5HT receptors... study
« Reply #1 on: May 30th, 2003, 12:04pm » |
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This post and the previous one (twin study) suggest the possibilty of an anomoly in the gene (or genes) which encode for the 5HT1D receptor, or even an anomoly in the gene which encodes serotonin transporter proteins.
In fact, in 1996, NIH researchers reported finding a repeated stretch of DNA in the gene that encodes for the serotonin transporter protein. These researchers postulate that persons with shorter repeats in this gene may produce substandard quantities of the serotonin transport protein.
If that is the case, then longer repeats might produce too many of these proteins. If too many of these transporter proteins are present and active in the synapse, then serotonin could be swept from the synapse by these proteins at too rapid a rate. This action could prevent an adequate amount of serotonin from settling into the serotonin receptors.
More wild speculation. If the production of these proteins is regulated according to circadean rhythm (which the hypothalamus influences) maybe these proteins are being produced and released too often, in direct relation with the anomoly in the circadean rhythm.
PFDANs
-Curtis
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