Background: In earlier posts we described how commensal bacteria in the gut regulates the induction of T regulatory cells called Tregs that are important for immune functions. The loss of which may include autoimmune-type expressions and may be influential in MCS by loss of tolerance. In addition, we have also discussed how cortico-releasing hormone (CRH or CRF) has many effects and tissue targets, can be influenced by odors, may influence addictive-type behaviors and abherrant signaling may lead to altered signaling that can lead to mood disorders and have other negative influences on behaviors. The activation of CRH is part of the stress response and therefore, become an important part of the response to environmental cues. This same response activates the inflammatory cascade and therefore, the existence of one may coincide with the activation of the other. In addition, inflammatory cascades include activation of immune cells including mast cells.
Christy and Brown explain that Tregs are important in autoimmune disease and have the potential upon induction to prevent and reverse these conditions including diabetes and multiple sclerosis. Both of which are now considered to have an environmental connection. In addition the author notes that lupus, another condition with possible environmental triggers, and other autoimmune conditions are not just a loss of Tregs but a condition where other immune cells called Ag-effector cells become resistent to Treg suppression. At this point, one would suggest that other physiological pathways may be involved and this potentiates the non-adaptive conditions that lead to MCS. In other blogs, we have discussed a number of these conditions including nutrition and expression of cytokines, as well as, the expression of Nrf2.
Christy and Brown also present another important factor that very well may influence the development of MCS by contributing to loss of tolerance and that is the production of CRH from mast cells. These cells are often produced from inflammatory reactions such as those conditions that produced and reported from environmental toxin exposure. The authors discuss how the role of CRH produced from these inflammatory cells in basically an uptapped area of immune science. On the other hand, Soderholm does note that mast cells and CRH are implicated in disruptions of barrier function in irritable bowel syndrome and to a degree, it it now understood they are produced in inflamed tissue and increase inflammation. This protein has been implicated in reactions in rheumatoid arthritis and other inflammatory conditions during stress. For this reason, one can suggest that inflammatory conditions and production of mast cells which can produce this protein may contribute to the response and long-term activation can have important effects on downstream targets and participate in autoimmune-type response such as those observed in chemical sensitivities.
Past HEIRS Blogs: Related Tags: CRF , CRH , Nrf2
Christy, A. L. and Brown, M. A. (2007). The multitasking mast cell: Positive and negative roles in the progression of autoimmunity. J Immunol, 179(5):2673-2679.
http://www.citeulike.org/user/HEIRS/article/7357936
McKay, D. M. (2005). Good bug, bad bug: in the case of enteric inflammatory disease does the epithelium decide? Memórias do Instituto Oswaldo Cruz, 100(s1):205-210.
http://www.citeulike.org/user/HEIRS/article/7357955
Teitelbaum, A. A., Gareau, M. G., Jury, J., Yang, P. C., and Perdue, M. H. (2008). Chronic peripheral administration of corticotropin-releasing factor causes colonic barrier dysfunction similar to psychological stress. Am J Physiol Gastrointest Liver Physiol, 295(3):G452-459. http://www.citeulike.org/user/HEIRS/article/7357961
Showing posts with label CRF. Show all posts
Showing posts with label CRF. Show all posts
Thursday, June 24, 2010
Thursday, June 10, 2010
Effect of CRH on NO bioavailability, ROS production and antioxidant defense systems in endothelial EAhy926 cells.
The data indicate that CRH may act as a regulator of pro-inflammatory mechanisms inducing adaptation of endothelial cell function to local stress.
"Gougoura, S., Liakos, P., and Koukoulis, G. N. (2010). Effect of crh on no bioavailability, ros production and antioxidant defense systems in endothelial eahy926 cells. Free radical research, 44(7):803-812."
CiteULike: Effect of CRH on NO bioavailability, ROS production and antioxidant defense systems in endothelial EAhy926 cells.:
Sunday, May 23, 2010
Gulf War and Health: Links to Fibromalgia, PTSD, IBS
IOM determines that Gulf War service causes post-traumatic stress disorder (PTSD) and that service is associated with multisymptom illness; gastrointestinal disorders such as irritable bowel syndrome; alcohol and other substance abuse; and anxiety disorders and other psychiatric disorders. To ensure that our veterans receive the best possible care, now and in the future, the government should continue to monitor their health and conduct research to identify the best treatments to assist Gulf War veterans still suffering from persistent, unexplained illnesses. The report also says there is some limited evidence of a link to fibromyalgia and ALS but the connection is less clear. Read more.
Il-6 Modulates CRF in the Hypothalamus in Response to Different Signals.
Module: 5/22/2010
Background: CRF can regulate signaling in response to different odors. In those cases, it can lead to an anxiolytic or elevation and other responses typical of the stress response including pain generation, immune regulation, itch, rash and other changes such as gastric function alterations. Of course, these are symptoms characteristic of chemical sensitivity and also some symptoms characteristic of other environmentally influenced conditions such as CFS and sickness syndrome.
A major regulator of sickness syndrome is Il-6 which can be functionally modulated through Il-10 and ultimately most probably HO-1 which has been shown in other studies to increase during exercise. Interestingly, one can identify similarities in cancer-related fatigue to some chronic symptoms of CFS and sickness syndrome including the exhausting fatigue and cachexia that is exhibited in the latter, in animals and humans. Preliminary studies suggest cytokine Il-6/Il-8 may modulate the severity of cancer-related fatigue and others show cancer-related fatigue is common with serotonin dysregulation. Coincidentally, in the trout corticotrophin activation by ammonia is associated with alterations in neurotransmitter levels including dopamine and serotonin. So here again, we see potential especially with periods of aberrant corticotrophin signalling, where symptoms of environmental illness such as anxiety, depression, weakeness and fatigue may present itself. These findings supports past studies that suggest that fatigue in CFS may be in part due to serotonin dysregulation and elevations in Il-6.(Ryan)
CiteULike: Transcriptional regulation of hypothalamic corticotropin-releasing factor gene.: "Glucocorticoid-dependent repression of cAMP-stimulated CRF promoter activity is mediated by both nGRE and SRE in hypothalamic cells. Interleukin (IL)-6 produced in the hypothalamus stimulates the CRF gene. Suppressor of cytokine signaling-3, which is induced by a cAMP stimulant and IL-6, is involved in the negative regulation of CRF gene expression in hypothalamic cells. Such complex mechanisms would contribute to stress responses and homeostasis in the hypothalamus."
Related: Hummel, M., Cummons, T., Lu, P., Mark, L., Harrison, J. E., Kennedy, J. D., and Whiteside, G. T. (2010). Pain is a salient ßtressor" that is mediated by corticotropin- releasing factor-1 receptors. Neuropharmacology.
http://www.citeulike.org/user/HEIRS/article/7177466
Coric, V., Feldman, H. H., Oren, D. A., Shekhar, A., Pultz, J., Dockens, R. C., Wu, X., Gentile, K. A., Huang, S.-P. P., Emison, E., Delmonte, T., D'Souza, B. B., Zimbroff, D. L., Grebb, J. A., Goddard, A. W., and Stock, E. G. (2010). Multicenter, randomized, double-blind, active comparator and placebo-controlled trial of a corticotropin-releasing factor receptor-1 antagonist in generalized anxiety disorder. Depression and anxiety, 27(5):417-425.
http://www.citeulike.org/user/HEIRS/article/7193107
Theoharides, T. C., Singh, Boucher, W., Pang, X., Letourneau, R., Webster, E., and Chrousos, G. (1998). Corticotropin-releasing hormone induces skin mast cell degranulation and increased vascular permeability, a possible explanation for its proinflammatory effects. Endocrinology, 139(1):403-413.
http://www.citeulike.org/user/HEIRS/article/7207688
Mustian, K. M., Fisher, S., Adams, J., Janelsins, M., Palesh, O., Darling, T., Peppone, L., Heckler, C., Williams, J., and Morrow, G. (2009). Cytokine-mediated changes associated with improvements in cancer-related fatigue induced by exercise: Results from a randomized pilot study of cancer patients receiving radiotherapy. Journal of Clinical Oncology, 27(15s).
http://www.citeulike.org/user/HEIRS/article/7207720
Ryan, J. L., Carroll, J. K., Ryan, E. P., Mustian, K. M., Fiscell, K., and Morrow, G. R. (2007). Mechanisms of cancer-related fatigue. The Oncologist, 12(1 supp):22-34.
http://www.citeulike.org/user/HEIRS/article/7207823
Background: CRF can regulate signaling in response to different odors. In those cases, it can lead to an anxiolytic or elevation and other responses typical of the stress response including pain generation, immune regulation, itch, rash and other changes such as gastric function alterations. Of course, these are symptoms characteristic of chemical sensitivity and also some symptoms characteristic of other environmentally influenced conditions such as CFS and sickness syndrome.
A major regulator of sickness syndrome is Il-6 which can be functionally modulated through Il-10 and ultimately most probably HO-1 which has been shown in other studies to increase during exercise. Interestingly, one can identify similarities in cancer-related fatigue to some chronic symptoms of CFS and sickness syndrome including the exhausting fatigue and cachexia that is exhibited in the latter, in animals and humans. Preliminary studies suggest cytokine Il-6/Il-8 may modulate the severity of cancer-related fatigue and others show cancer-related fatigue is common with serotonin dysregulation. Coincidentally, in the trout corticotrophin activation by ammonia is associated with alterations in neurotransmitter levels including dopamine and serotonin. So here again, we see potential especially with periods of aberrant corticotrophin signalling, where symptoms of environmental illness such as anxiety, depression, weakeness and fatigue may present itself. These findings supports past studies that suggest that fatigue in CFS may be in part due to serotonin dysregulation and elevations in Il-6.(Ryan)
CiteULike: Transcriptional regulation of hypothalamic corticotropin-releasing factor gene.: "Glucocorticoid-dependent repression of cAMP-stimulated CRF promoter activity is mediated by both nGRE and SRE in hypothalamic cells. Interleukin (IL)-6 produced in the hypothalamus stimulates the CRF gene. Suppressor of cytokine signaling-3, which is induced by a cAMP stimulant and IL-6, is involved in the negative regulation of CRF gene expression in hypothalamic cells. Such complex mechanisms would contribute to stress responses and homeostasis in the hypothalamus."
Related: Hummel, M., Cummons, T., Lu, P., Mark, L., Harrison, J. E., Kennedy, J. D., and Whiteside, G. T. (2010). Pain is a salient ßtressor" that is mediated by corticotropin- releasing factor-1 receptors. Neuropharmacology.
http://www.citeulike.org/user/HEIRS/article/7177466
Coric, V., Feldman, H. H., Oren, D. A., Shekhar, A., Pultz, J., Dockens, R. C., Wu, X., Gentile, K. A., Huang, S.-P. P., Emison, E., Delmonte, T., D'Souza, B. B., Zimbroff, D. L., Grebb, J. A., Goddard, A. W., and Stock, E. G. (2010). Multicenter, randomized, double-blind, active comparator and placebo-controlled trial of a corticotropin-releasing factor receptor-1 antagonist in generalized anxiety disorder. Depression and anxiety, 27(5):417-425.
http://www.citeulike.org/user/HEIRS/article/7193107
Theoharides, T. C., Singh, Boucher, W., Pang, X., Letourneau, R., Webster, E., and Chrousos, G. (1998). Corticotropin-releasing hormone induces skin mast cell degranulation and increased vascular permeability, a possible explanation for its proinflammatory effects. Endocrinology, 139(1):403-413.
http://www.citeulike.org/user/HEIRS/article/7207688
Mustian, K. M., Fisher, S., Adams, J., Janelsins, M., Palesh, O., Darling, T., Peppone, L., Heckler, C., Williams, J., and Morrow, G. (2009). Cytokine-mediated changes associated with improvements in cancer-related fatigue induced by exercise: Results from a randomized pilot study of cancer patients receiving radiotherapy. Journal of Clinical Oncology, 27(15s).
http://www.citeulike.org/user/HEIRS/article/7207720
Ryan, J. L., Carroll, J. K., Ryan, E. P., Mustian, K. M., Fiscell, K., and Morrow, G. R. (2007). Mechanisms of cancer-related fatigue. The Oncologist, 12(1 supp):22-34.
http://www.citeulike.org/user/HEIRS/article/7207823
Saturday, May 15, 2010
How odors activate the stress response and inflammatory mediators!
"enhanced IL-6 activity may stimulate the HPA axis at the level of the hypothalamus via a CRH-mediated mechanism For example, inhalation of citralva, a sample used during the study, may enhance the stress response or may itself act as a stress."
Effects of Odorants on the Hypothalamic-Pituitary-Adrenal Axis and Interleukin-6 (IL-6) and IL-6 Receptor mRNA Expression in Rat Hypothalamus after Restraint Stress -- Komori et al. 28 (9): 767 -- Chemical Senses: "enhanced IL-6 activity may stimulate the HPA axis at the level of the hypothalamus (Naitoh et al., 1988; Fukata et al., 1989; Navarra et al., 1991; Tominaga et al., 1991) via a CRH-mediated mechanism (Navarra et al., 1991; Lyson and McCann, 1992), i.e. inhalation of citralva may enhance the stress response or may itself act as a stress."
Effects of Odorants on the Hypothalamic-Pituitary-Adrenal Axis and Interleukin-6 (IL-6) and IL-6 Receptor mRNA Expression in Rat Hypothalamus after Restraint Stress -- Komori et al. 28 (9): 767 -- Chemical Senses: "enhanced IL-6 activity may stimulate the HPA axis at the level of the hypothalamus (Naitoh et al., 1988; Fukata et al., 1989; Navarra et al., 1991; Tominaga et al., 1991) via a CRH-mediated mechanism (Navarra et al., 1991; Lyson and McCann, 1992), i.e. inhalation of citralva may enhance the stress response or may itself act as a stress."
Pathway Impairment that Regulates Stress Response Could Lead to A Variety of Environmental Diseases
A recent study determined that caffeine can be a preventative against some of the health effects in Parkinson's disease caused by pesticides. The following pathway is a good representation of the NO/cGMP pathway that is more than likely effected by caffeine in these conditions and can account for some of the locomoter problems in PD. As one can see, expression of other proteins including BDNF rely on its activity. In other blogs, we have noted that BDNF is altered in environmental illnesses including CFS and may account for mood changes that occur with the condition. Proper signaling of the NO/cGMP pathway is important for a number of health conditions because the pathways are consistently activated by a number of different xenobiotics and environmental cues.
Alterations in the functioning of Nrf2 and other conditions like excretory defects that increase ammonia levels with negatively impact this system. While NO is an important component of this pathway - the actual dysfunction is not related to peroxynitrite, although oxidative stress to some may increase dysfunction though loss of NO signalling. Madhusoodanan explains that in this case, "nitric oxide is a short lived free radical species synthesized by NOS. The physiological role of NO depends on its local concentration as wells as the availability of downstream targets. At low levels, activation of guanalyl cyclase is the major event by NO. The resulting elevation of cGMP serves as an regulator of many events." I suggest that many environmental diseases including CFS and MCS are probably due more to the impairments of NO/cGMP which is also negatively effected by endogenous gases including ammonia and the impairment of the system results in astrocyte damage. Because Nrf2 is also neuroprotective --- alterations in Nrf2 will contribute to neural injury. Also, cGMP inhibits the protein GSK-3b which is an off/on switch for Nrf2. Studies have demonstrated that Nrf2 regulates the antioxidant complexes of HO-1/CO which modulates CRF (which can be activated by odors) and CO activates cGMP. These pathways seem to strongly suggest that Nrf2 ultimately may influence the regulation of the stress response from environmental cues. In any case, HO-1/CO does modulate the CRF system which can be activated by response cytokines such as Il-1.
Recent studies show that increasing Nrf2 may be beneficial in limiting neural injury and in this case, I would say it probably would too. The article discusses hormetic responses that we have also discussed at length and as Mattson describes "recent findings have elucidated hormetic mechanisms of action of phytochemicals (e.g., resveratrol, curcumin, sulforaphanes and catechins) using cell culture and animal models of neurological disorders. Examples of hormesis pathways activated by phytochemicals include the transcription factor Nrf-2 which activates genes controlled by the antioxidant response element, and histone deacetylases of the sirtuin family and FOXO transcription factors." This of course may act on activities involved in methylation.
Notes:
Madhusoodanan, K. and Murad, F. (2007). No-cgmp signaling and regenerative medicine involving stem cells. Neurochemical Research, 32(4):681-694.
http://www.citeulike.org/user/HEIRS/article/1245237
Chan, M.-H., Chien, T.-H., Lee, P.-Y., and Chen, H.-H. (2004). Involvement of no/cgmp pathway in toluene-induced locomotor hyperactivity in female rats. Psychopharmacology, 176(3):435-439.
http://www.citeulike.org/user/HEIRS/article/7170771
van Staveren, W. (2001). The effects of phosphodiesterase inhibition on cyclic gmp and cyclic amp accumulation in the hippocampus of the rat. Brain Research, 888(2):275-286.
http://www.citeulike.org/user/HEIRS/article/7170748
Kachroo, A., Irizarry, M. C., and Schwarzschild, M. A. (2010). Caffeine protects against combined paraquat and maneb-induced dopaminergic neuron degeneration. Experimental neurology, 223(2):657-661.
http://www.citeulike.org/user/HEIRS/article/6835294
Mattson, M. P., Son, T. G., and Camandola, S. (2007). Viewpoint: mechanisms of action and therapeutic potential of neurohormetic phytochemicals. Dose-response : a publication of International Hormesis Society, 5(3):174-186.
http://www.citeulike.org/user/HEIRS/article/3812627
Angulo, J., González-Corrochano, R., Cuevas, P., Fernández, A., Fuente, J. L. M., Rolo, F., Allona, A., and Sáenz de Tejada, I. (2009). Diabetes exacerbates the functional deficiency of no/cgmp pathway associated with erectile dysfunction in human corpus cavernosum and penile arteries. The journal of sexual medicine. http://www.citeulike.org/user/HEIRS/article/7170872
Yang, R., Wang, J., Chen, Y., Sun, Z., Wang, R., and Dai, Y. (2008). Effect of caffeine on erectile function via up-regulating cavernous cyclic guanosine monophosphate in diabetic rats. J Androl, 29(5):586-591. http://www.citeulike.org/user/HEIRS/article/7170883
Nisoli, E. and Carruba, M. O. (2006). Nitric oxide and mitochondrial biogenesis. J Cell Sci, 119(14):2855-2862.http://www.citeulike.org/user/HEIRS/article/7170901
Alterations in the functioning of Nrf2 and other conditions like excretory defects that increase ammonia levels with negatively impact this system. While NO is an important component of this pathway - the actual dysfunction is not related to peroxynitrite, although oxidative stress to some may increase dysfunction though loss of NO signalling. Madhusoodanan explains that in this case, "nitric oxide is a short lived free radical species synthesized by NOS. The physiological role of NO depends on its local concentration as wells as the availability of downstream targets. At low levels, activation of guanalyl cyclase is the major event by NO. The resulting elevation of cGMP serves as an regulator of many events." I suggest that many environmental diseases including CFS and MCS are probably due more to the impairments of NO/cGMP which is also negatively effected by endogenous gases including ammonia and the impairment of the system results in astrocyte damage. Because Nrf2 is also neuroprotective --- alterations in Nrf2 will contribute to neural injury. Also, cGMP inhibits the protein GSK-3b which is an off/on switch for Nrf2. Studies have demonstrated that Nrf2 regulates the antioxidant complexes of HO-1/CO which modulates CRF (which can be activated by odors) and CO activates cGMP. These pathways seem to strongly suggest that Nrf2 ultimately may influence the regulation of the stress response from environmental cues. In any case, HO-1/CO does modulate the CRF system which can be activated by response cytokines such as Il-1.
Recent studies show that increasing Nrf2 may be beneficial in limiting neural injury and in this case, I would say it probably would too. The article discusses hormetic responses that we have also discussed at length and as Mattson describes "recent findings have elucidated hormetic mechanisms of action of phytochemicals (e.g., resveratrol, curcumin, sulforaphanes and catechins) using cell culture and animal models of neurological disorders. Examples of hormesis pathways activated by phytochemicals include the transcription factor Nrf-2 which activates genes controlled by the antioxidant response element, and histone deacetylases of the sirtuin family and FOXO transcription factors." This of course may act on activities involved in methylation.
Notes:
- Diabetes exacerbates functional deficiency of NO/cGMP in ED
Madhusoodanan, K. and Murad, F. (2007). No-cgmp signaling and regenerative medicine involving stem cells. Neurochemical Research, 32(4):681-694.
http://www.citeulike.org/user/HEIRS/article/1245237
Chan, M.-H., Chien, T.-H., Lee, P.-Y., and Chen, H.-H. (2004). Involvement of no/cgmp pathway in toluene-induced locomotor hyperactivity in female rats. Psychopharmacology, 176(3):435-439.
http://www.citeulike.org/user/HEIRS/article/7170771
van Staveren, W. (2001). The effects of phosphodiesterase inhibition on cyclic gmp and cyclic amp accumulation in the hippocampus of the rat. Brain Research, 888(2):275-286.
http://www.citeulike.org/user/HEIRS/article/7170748
Kachroo, A., Irizarry, M. C., and Schwarzschild, M. A. (2010). Caffeine protects against combined paraquat and maneb-induced dopaminergic neuron degeneration. Experimental neurology, 223(2):657-661.
http://www.citeulike.org/user/HEIRS/article/6835294
Mattson, M. P., Son, T. G., and Camandola, S. (2007). Viewpoint: mechanisms of action and therapeutic potential of neurohormetic phytochemicals. Dose-response : a publication of International Hormesis Society, 5(3):174-186.
http://www.citeulike.org/user/HEIRS/article/3812627
Angulo, J., González-Corrochano, R., Cuevas, P., Fernández, A., Fuente, J. L. M., Rolo, F., Allona, A., and Sáenz de Tejada, I. (2009). Diabetes exacerbates the functional deficiency of no/cgmp pathway associated with erectile dysfunction in human corpus cavernosum and penile arteries. The journal of sexual medicine. http://www.citeulike.org/user/HEIRS/article/7170872
Yang, R., Wang, J., Chen, Y., Sun, Z., Wang, R., and Dai, Y. (2008). Effect of caffeine on erectile function via up-regulating cavernous cyclic guanosine monophosphate in diabetic rats. J Androl, 29(5):586-591. http://www.citeulike.org/user/HEIRS/article/7170883
Nisoli, E. and Carruba, M. O. (2006). Nitric oxide and mitochondrial biogenesis. J Cell Sci, 119(14):2855-2862.http://www.citeulike.org/user/HEIRS/article/7170901
Thursday, May 13, 2010
Is This a Plausible Mechanism for Multiple Chemical Sensitivity Responses?
The results of this study suggest that "electrical or chemical stimulation of the dorsal periaqueductal gray matter (DPAG) evokes escape, defensive behavior that has been related to panic attacks and that serotonin signaling may influence the panic behavior."
"Considering the triggers, this seems like a very plausible explanation for the mechanism or something similar in multiple chemical sensitivity. This area seems to be influenced by stress signalling and also interacts with certain proteins including the CRH which reacts to environmental cues that leads to changes in neurotransmission. According to one source, "periaqueductal gray matter is responsible for inhibiting nociceptive activity (often leading to pain) though the release of certain proteins. Nociceptive signaling forms a platform for the "central sensitization" in fibromyalgia and other pain conditions and involves the enhancement of impulses and dysfunction in the pain system." For this reason, it very well could be an important component in the responses associated with chemical sensitivity.(Spaeth) As far as fibromyalgia, alterations in serotonin have been noted in past studies.
CiteULike: Dorsal raphe nucleus regulation of a panic-like defensive behavior evoked by chemical stimulation of the rat dorsal periaqueductal gray matter.: "Miguel, T. L. B. L., Pobbe, R. L. H. L., Junior, A. S. S., and Junior, H. Z. Z. (2010). Dorsal raphe nucleus regulation of a panic-like defensive behavior evoked by chemical stimulation of the rat dorsal periaqueductal gray matter. Behavioural brain research."
Sources:
The Neurochemical Response Patterns to Acute Stress. Retrieved on May 13, 2010. http://focus.psychiatryonline.org/cgi/content/full/2/3/368/T1
Spaeth, M. (2006). Fibromyalgia syndrome: The role of neurochemicals. Primary Psychiatry, 13(9):72-75.
http://www.citeulike.org/user/HEIRS/article/7167665
"Considering the triggers, this seems like a very plausible explanation for the mechanism or something similar in multiple chemical sensitivity. This area seems to be influenced by stress signalling and also interacts with certain proteins including the CRH which reacts to environmental cues that leads to changes in neurotransmission. According to one source, "periaqueductal gray matter is responsible for inhibiting nociceptive activity (often leading to pain) though the release of certain proteins. Nociceptive signaling forms a platform for the "central sensitization" in fibromyalgia and other pain conditions and involves the enhancement of impulses and dysfunction in the pain system." For this reason, it very well could be an important component in the responses associated with chemical sensitivity.(Spaeth) As far as fibromyalgia, alterations in serotonin have been noted in past studies.
CiteULike: Dorsal raphe nucleus regulation of a panic-like defensive behavior evoked by chemical stimulation of the rat dorsal periaqueductal gray matter.: "Miguel, T. L. B. L., Pobbe, R. L. H. L., Junior, A. S. S., and Junior, H. Z. Z. (2010). Dorsal raphe nucleus regulation of a panic-like defensive behavior evoked by chemical stimulation of the rat dorsal periaqueductal gray matter. Behavioural brain research."
Sources:
The Neurochemical Response Patterns to Acute Stress. Retrieved on May 13, 2010. http://focus.psychiatryonline.org/cgi/content/full/2/3/368/T1
Spaeth, M. (2006). Fibromyalgia syndrome: The role of neurochemicals. Primary Psychiatry, 13(9):72-75.
http://www.citeulike.org/user/HEIRS/article/7167665
Monday, February 1, 2010
Hyperammonemia, Subordination, Hypoxia Influence Stress Hormone CRF Production in Fish
"Comparison of the plasma cortisol levels in response to the diverse treatments showed that subordination was the most severe stressor followed by hyperammonemia, isolation, and hypoxia. In the POA, with the exception of subordination that had no effect on UI expression, all stressors resulted in increase in CRF and UI mRNA levels."
Comment: Basically, this says that in fish these stressors increase stress hormones. Other organisms are often used as experimental models to test psychological theories. These same hormonal pathways exist in humans and for this reason, one can suggest these stressors may elicit similar responses and these kinds of experiments are often performed on animals to analyze reactions before humans or where experimentation on humans would be "unethical" or "too difficult".
Bernier, N. J., Alderman, S. L., and Bristow, E. N. (2008). Heads or tails? stressor-specific expression of corticotropin-releasing factor and urotensin i in the preoptic area and caudal neurosecretory system of rainbow trout. The Journal of endocrinology, 196(3):637-648. http://www.citeulike.org/user/HEIRS/article/6611532
Kawabata, K., Kawai, Y., and Terao, J. (2009). Suppressive effect of quercetin on acute stress-induced hypothalamic-pituitary-adrenal axis response in wistar rats. The Journal of nutritional biochemistry. http://www.citeulike.org/user/HEIRS/article/4498837
Ortega, V. A., Renner, K. J., and Bernier, N. J. (2005). Appetite-suppressing effects of ammonia exposure in rainbow trout associated with regional and temporal activation of brain monoaminergic and crf systems. J Exp Biol, 208(10):1855-1866. http://www.citeulike.org/user/HEIRS/article/6594636
Land, B. B., Bruchas, M. R., Lemos, J. C., Xu, M., Melief, E. J., and Chavkin, C. (2008). The dysphoric component of stress is encoded by activation of the dynorphin kappa-opioid system. J. Neurosci., 28(2):407-414. http://www.citeulike.org/user/HEIRS/article/2215488
Walsh, P. J., Veauvy, C. M., McDonald, M. D., Pamenter, M. E., Buck, L. T., and Wilkie, M. P. (2007). Piscine insights into comparisons of anoxia tolerance, ammonia toxicity, stroke and hepatic encephalopathy. Comparative biochemistry and physiology. Part A, Molecular & integrative physiology, 147(2):332-343. http://www.citeulike.org/user/HEIRS/article/6611593
Comment: Basically, this says that in fish these stressors increase stress hormones. Other organisms are often used as experimental models to test psychological theories. These same hormonal pathways exist in humans and for this reason, one can suggest these stressors may elicit similar responses and these kinds of experiments are often performed on animals to analyze reactions before humans or where experimentation on humans would be "unethical" or "too difficult".
Bernier, N. J., Alderman, S. L., and Bristow, E. N. (2008). Heads or tails? stressor-specific expression of corticotropin-releasing factor and urotensin i in the preoptic area and caudal neurosecretory system of rainbow trout. The Journal of endocrinology, 196(3):637-648. http://www.citeulike.org/user/HEIRS/article/6611532
Kawabata, K., Kawai, Y., and Terao, J. (2009). Suppressive effect of quercetin on acute stress-induced hypothalamic-pituitary-adrenal axis response in wistar rats. The Journal of nutritional biochemistry. http://www.citeulike.org/user/HEIRS/article/4498837
Ortega, V. A., Renner, K. J., and Bernier, N. J. (2005). Appetite-suppressing effects of ammonia exposure in rainbow trout associated with regional and temporal activation of brain monoaminergic and crf systems. J Exp Biol, 208(10):1855-1866. http://www.citeulike.org/user/HEIRS/article/6594636
Land, B. B., Bruchas, M. R., Lemos, J. C., Xu, M., Melief, E. J., and Chavkin, C. (2008). The dysphoric component of stress is encoded by activation of the dynorphin kappa-opioid system. J. Neurosci., 28(2):407-414. http://www.citeulike.org/user/HEIRS/article/2215488
Walsh, P. J., Veauvy, C. M., McDonald, M. D., Pamenter, M. E., Buck, L. T., and Wilkie, M. P. (2007). Piscine insights into comparisons of anoxia tolerance, ammonia toxicity, stroke and hepatic encephalopathy. Comparative biochemistry and physiology. Part A, Molecular & integrative physiology, 147(2):332-343. http://www.citeulike.org/user/HEIRS/article/6611593
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