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Dysmorphic contribution of neurotransmitter and neuroendocrine system polymorphisms to subtherapeutic mood states
OBJECTIVE: From an evolutionary perspective, emotions emerged as rapid adaptive reactions that increase survival rates. Current psychobiology includes the consideration that genetic changes affecting neuroendocrine and neurotransmission pathways may also be affecting mood states. Following this hypo...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6379594/ https://www.ncbi.nlm.nih.gov/pubmed/30656852 http://dx.doi.org/10.1002/brb3.1140 |
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author | Gonzalez, Irene Polvillo, Rocio Ruiz‐Galdon, Maximiliano Reyes‐Engel, Armando Royo, Jose Luis |
author_facet | Gonzalez, Irene Polvillo, Rocio Ruiz‐Galdon, Maximiliano Reyes‐Engel, Armando Royo, Jose Luis |
author_sort | Gonzalez, Irene |
collection | PubMed |
description | OBJECTIVE: From an evolutionary perspective, emotions emerged as rapid adaptive reactions that increase survival rates. Current psychobiology includes the consideration that genetic changes affecting neuroendocrine and neurotransmission pathways may also be affecting mood states. Following this hypothesis, abnormal levels of any of the aminergic neurotransmitters would be of considerable importance in the development of a pathophysiological state. MATERIALS AND METHODS: A total of 668 students from the School of Medicine of the University of Malaga (Average = 22.41 ± 3; 41% men) provided self‐report measures of mood states using POMS and GHQ‐28 questionnaires and buccal cells for genotyping 19 polymorphisms from 14 selected neurotransmitter pathways genes (HTR1A; HTR2A; HTR2C; HTR3B; TPH1; SLC18A1; SLC18A2; COMT; MAOA; MAOB) and neuroendocrine system (AVPR1B; OPRM1; BDNF; OXTR). RESULTS: MAOA rs3788862 genotype correlates with decreasing levels of Tension among females (beta = −0.168, p‐value = 0.003) but it is neutral among males in this subscale. On the contrary, it correlates with lower GHQ‐28 depression scores among males (beta = −0.196, p‐value = 0.008). Equivalently, SLC18A1 and HTR2A variants correlated with anger and vigor scores, only among males. From the neuroendocrine system, OPRM1 rs1799971 correlated increasing levels of female's Anxiety, depression and Social Dysfunction scores. CONCLUSION: Our findings suggest that these polymorphisms contribute to define general population mood levels, although exhibiting a clear sexual dimorphism. |
format | Online Article Text |
id | pubmed-6379594 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-63795942019-02-28 Dysmorphic contribution of neurotransmitter and neuroendocrine system polymorphisms to subtherapeutic mood states Gonzalez, Irene Polvillo, Rocio Ruiz‐Galdon, Maximiliano Reyes‐Engel, Armando Royo, Jose Luis Brain Behav Original Research OBJECTIVE: From an evolutionary perspective, emotions emerged as rapid adaptive reactions that increase survival rates. Current psychobiology includes the consideration that genetic changes affecting neuroendocrine and neurotransmission pathways may also be affecting mood states. Following this hypothesis, abnormal levels of any of the aminergic neurotransmitters would be of considerable importance in the development of a pathophysiological state. MATERIALS AND METHODS: A total of 668 students from the School of Medicine of the University of Malaga (Average = 22.41 ± 3; 41% men) provided self‐report measures of mood states using POMS and GHQ‐28 questionnaires and buccal cells for genotyping 19 polymorphisms from 14 selected neurotransmitter pathways genes (HTR1A; HTR2A; HTR2C; HTR3B; TPH1; SLC18A1; SLC18A2; COMT; MAOA; MAOB) and neuroendocrine system (AVPR1B; OPRM1; BDNF; OXTR). RESULTS: MAOA rs3788862 genotype correlates with decreasing levels of Tension among females (beta = −0.168, p‐value = 0.003) but it is neutral among males in this subscale. On the contrary, it correlates with lower GHQ‐28 depression scores among males (beta = −0.196, p‐value = 0.008). Equivalently, SLC18A1 and HTR2A variants correlated with anger and vigor scores, only among males. From the neuroendocrine system, OPRM1 rs1799971 correlated increasing levels of female's Anxiety, depression and Social Dysfunction scores. CONCLUSION: Our findings suggest that these polymorphisms contribute to define general population mood levels, although exhibiting a clear sexual dimorphism. John Wiley and Sons Inc. 2019-01-17 /pmc/articles/PMC6379594/ /pubmed/30656852 http://dx.doi.org/10.1002/brb3.1140 Text en © 2018 The Authors. Brain and Behavior published by Wiley Periodicals, Inc. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research Gonzalez, Irene Polvillo, Rocio Ruiz‐Galdon, Maximiliano Reyes‐Engel, Armando Royo, Jose Luis Dysmorphic contribution of neurotransmitter and neuroendocrine system polymorphisms to subtherapeutic mood states |
title | Dysmorphic contribution of neurotransmitter and neuroendocrine system polymorphisms to subtherapeutic mood states |
title_full | Dysmorphic contribution of neurotransmitter and neuroendocrine system polymorphisms to subtherapeutic mood states |
title_fullStr | Dysmorphic contribution of neurotransmitter and neuroendocrine system polymorphisms to subtherapeutic mood states |
title_full_unstemmed | Dysmorphic contribution of neurotransmitter and neuroendocrine system polymorphisms to subtherapeutic mood states |
title_short | Dysmorphic contribution of neurotransmitter and neuroendocrine system polymorphisms to subtherapeutic mood states |
title_sort | dysmorphic contribution of neurotransmitter and neuroendocrine system polymorphisms to subtherapeutic mood states |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6379594/ https://www.ncbi.nlm.nih.gov/pubmed/30656852 http://dx.doi.org/10.1002/brb3.1140 |
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