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Serotonin regulation of the human stress response.
Psychoneuroendocrinology 2006; 31(9):1087-97P

Abstract

Acute tryptophan depletion (ATD) is a technique that has been used to evaluate the effects on humans of acutely reducing serotonin neurotransmission. We have developed a model using a single breath of 35% CO(2) that activates the hormonal axis and produces autonomic and behavioural arousal, thus modelling a stress response. This study combines ATD and single breath 35% CO(2) inhalation to study stress responses in volunteers. A randomised, double-blinded, placebo-controlled, cross-over trial involving 14 healthy adult volunteers aged between 18 and 65 years was undertaken. Subjects underwent double-blind tryptophan depletion over 2 days and were then crossed over 1 week later. During each study day, at the time of peak depletion, participants were single blinded to receive a single breath of 35% CO(2) or air. This was followed 40 min later by the other gas. Psychological outcomes were assessed with the Spielberger State Anxiety Inventory (SSAI), Visual Analogue Scales (VAS), Panic Inventory (PI), Panic and Agoraphobia Scale (PSI) and Beck Depression Inventory (BDI). Physiological outcome was measured by serial plasma cortisol, prolactin and tryptophan levels, pulse and blood pressure. Tryptophan depletion did not exacerbate 35% CO(2) inhalation effects on anxiety symptoms. Single breath CO(2) robustly increased plasma cortisol levels in comparison to an air inhalation; this was less certain for prolactin levels. ATD influenced the HPA axis (associated with higher cortisol levels), apparently independent of CO(2) or air inhalation stressors. ATD and 35% CO(2) inhalation both induced a pressor response and bradycardia in these normal volunteers. Thirty-five percent CO(2) inhalation and ATD independently activate the human stress response, but do not appear to produce synergistic effects when combined, at least for the conditions produced in this study.

Authors+Show Affiliations

School of Psychiatry and Clinical Neurosciences (M521), University of Western Australia, QEII Medical Centre, Perth, Nedlands, Western Australia 6009, Australia. sean.hood@uwa.edu.auNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Randomized Controlled Trial

Language

eng

PubMed ID

16962720

Citation

Hood, Sean D., et al. "Serotonin Regulation of the Human Stress Response." Psychoneuroendocrinology, vol. 31, no. 9, 2006, pp. 1087-97.
Hood SD, Hince DA, Robinson H, et al. Serotonin regulation of the human stress response. Psychoneuroendocrinology. 2006;31(9):1087-97.
Hood, S. D., Hince, D. A., Robinson, H., Cirillo, M., Christmas, D., & Kaye, J. M. (2006). Serotonin regulation of the human stress response. Psychoneuroendocrinology, 31(9), pp. 1087-97.
Hood SD, et al. Serotonin Regulation of the Human Stress Response. Psychoneuroendocrinology. 2006;31(9):1087-97. PubMed PMID: 16962720.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Serotonin regulation of the human stress response. AU - Hood,Sean D, AU - Hince,Dana A, AU - Robinson,Hayley, AU - Cirillo,Melita, AU - Christmas,David, AU - Kaye,Joey M, Y1 - 2006/09/08/ PY - 2006/05/05/received PY - 2006/07/06/revised PY - 2006/07/16/accepted PY - 2006/9/12/pubmed PY - 2006/12/9/medline PY - 2006/9/12/entrez SP - 1087 EP - 97 JF - Psychoneuroendocrinology JO - Psychoneuroendocrinology VL - 31 IS - 9 N2 - Acute tryptophan depletion (ATD) is a technique that has been used to evaluate the effects on humans of acutely reducing serotonin neurotransmission. We have developed a model using a single breath of 35% CO(2) that activates the hormonal axis and produces autonomic and behavioural arousal, thus modelling a stress response. This study combines ATD and single breath 35% CO(2) inhalation to study stress responses in volunteers. A randomised, double-blinded, placebo-controlled, cross-over trial involving 14 healthy adult volunteers aged between 18 and 65 years was undertaken. Subjects underwent double-blind tryptophan depletion over 2 days and were then crossed over 1 week later. During each study day, at the time of peak depletion, participants were single blinded to receive a single breath of 35% CO(2) or air. This was followed 40 min later by the other gas. Psychological outcomes were assessed with the Spielberger State Anxiety Inventory (SSAI), Visual Analogue Scales (VAS), Panic Inventory (PI), Panic and Agoraphobia Scale (PSI) and Beck Depression Inventory (BDI). Physiological outcome was measured by serial plasma cortisol, prolactin and tryptophan levels, pulse and blood pressure. Tryptophan depletion did not exacerbate 35% CO(2) inhalation effects on anxiety symptoms. Single breath CO(2) robustly increased plasma cortisol levels in comparison to an air inhalation; this was less certain for prolactin levels. ATD influenced the HPA axis (associated with higher cortisol levels), apparently independent of CO(2) or air inhalation stressors. ATD and 35% CO(2) inhalation both induced a pressor response and bradycardia in these normal volunteers. Thirty-five percent CO(2) inhalation and ATD independently activate the human stress response, but do not appear to produce synergistic effects when combined, at least for the conditions produced in this study. SN - 0306-4530 UR - https://www.unboundmedicine.com/medline/citation/16962720/Serotonin_regulation_of_the_human_stress_response_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4530(06)00132-6 DB - PRIME DP - Unbound Medicine ER -