Glial Activation and Expression of the Serotonin Transporter in Chronic Fatigue Syndrome
Fatigue is commonly reported in a variety of illnesses and has major impact on quality of life. Chronic fatigue syndrome (CFS) is a debilitating syndrome of unknown etiology. The clinical symptoms include problems in neuroendocrine, autonomic, and immune systems. It is becoming clear that the brain...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2018-11-01
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| Series: | Frontiers in Psychiatry |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/article/10.3389/fpsyt.2018.00589/full |
| _version_ | 1818620394644439040 |
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| author | Mami Noda Masataka Ifuku Md. Shamim Hossain Toshihiko Katafuchi |
| author_facet | Mami Noda Masataka Ifuku Md. Shamim Hossain Toshihiko Katafuchi |
| author_sort | Mami Noda |
| collection | DOAJ |
| description | Fatigue is commonly reported in a variety of illnesses and has major impact on quality of life. Chronic fatigue syndrome (CFS) is a debilitating syndrome of unknown etiology. The clinical symptoms include problems in neuroendocrine, autonomic, and immune systems. It is becoming clear that the brain is the central regulator of CFS. For example, neuroinflammation, especially induced by activation of microglia and astrocytes, may play a prominent role in the development of CFS, though little is known about molecular mechanisms. Many possible causes of CFS have been proposed. However, in this mini-review, we summarize evidence for a role for microglia and astrocytes in the onset and the maintenance of immunologically induced CFS. In a model using virus mimicking synthetic double-stranded RNA, infection causes sequential signaling such as increased blood brain barrier (BBB) permeability, microglia/macrophage activation through Toll-like receptor 3 (TLR3) signaling, secretion of IL-1β, upregulation of the serotonin transporter (5-HTT) in astrocytes, reducing extracellular serotonin (5-HT) levels and hence reduced activation of 5-HT1A receptor subtype. Hopefully, drug discovery targeting these pathways may be effective for CFS therapy. |
| first_indexed | 2024-12-16T17:52:41Z |
| format | Article |
| id | doaj.art-4bfe12b92b2f43268eb9d28ceb1226e5 |
| institution | Directory Open Access Journal |
| issn | 1664-0640 |
| language | English |
| last_indexed | 2024-12-16T17:52:41Z |
| publishDate | 2018-11-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Psychiatry |
| spelling | doaj.art-4bfe12b92b2f43268eb9d28ceb1226e52022-12-21T22:22:14ZengFrontiers Media S.A.Frontiers in Psychiatry1664-06402018-11-01910.3389/fpsyt.2018.00589398852Glial Activation and Expression of the Serotonin Transporter in Chronic Fatigue SyndromeMami Noda0Masataka Ifuku1Md. Shamim Hossain2Toshihiko Katafuchi3Laboratory of Pathophysiology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka, JapanDepartment of Neuroinflammation and Brain Fatigue Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, JapanDepartment of Neuroinflammation and Brain Fatigue Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, JapanDepartment of Neuroinflammation and Brain Fatigue Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka, JapanFatigue is commonly reported in a variety of illnesses and has major impact on quality of life. Chronic fatigue syndrome (CFS) is a debilitating syndrome of unknown etiology. The clinical symptoms include problems in neuroendocrine, autonomic, and immune systems. It is becoming clear that the brain is the central regulator of CFS. For example, neuroinflammation, especially induced by activation of microglia and astrocytes, may play a prominent role in the development of CFS, though little is known about molecular mechanisms. Many possible causes of CFS have been proposed. However, in this mini-review, we summarize evidence for a role for microglia and astrocytes in the onset and the maintenance of immunologically induced CFS. In a model using virus mimicking synthetic double-stranded RNA, infection causes sequential signaling such as increased blood brain barrier (BBB) permeability, microglia/macrophage activation through Toll-like receptor 3 (TLR3) signaling, secretion of IL-1β, upregulation of the serotonin transporter (5-HTT) in astrocytes, reducing extracellular serotonin (5-HT) levels and hence reduced activation of 5-HT1A receptor subtype. Hopefully, drug discovery targeting these pathways may be effective for CFS therapy.https://www.frontiersin.org/article/10.3389/fpsyt.2018.00589/fullchronic fatigue syndromepoly I:CTLR3IL-1betaserotonin transporter |
| spellingShingle | Mami Noda Masataka Ifuku Md. Shamim Hossain Toshihiko Katafuchi Glial Activation and Expression of the Serotonin Transporter in Chronic Fatigue Syndrome Frontiers in Psychiatry chronic fatigue syndrome poly I:C TLR3 IL-1beta serotonin transporter |
| title | Glial Activation and Expression of the Serotonin Transporter in Chronic Fatigue Syndrome |
| title_full | Glial Activation and Expression of the Serotonin Transporter in Chronic Fatigue Syndrome |
| title_fullStr | Glial Activation and Expression of the Serotonin Transporter in Chronic Fatigue Syndrome |
| title_full_unstemmed | Glial Activation and Expression of the Serotonin Transporter in Chronic Fatigue Syndrome |
| title_short | Glial Activation and Expression of the Serotonin Transporter in Chronic Fatigue Syndrome |
| title_sort | glial activation and expression of the serotonin transporter in chronic fatigue syndrome |
| topic | chronic fatigue syndrome poly I:C TLR3 IL-1beta serotonin transporter |
| url | https://www.frontiersin.org/article/10.3389/fpsyt.2018.00589/full |
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