Reduction of serotonin transporters of patients with chronic fatigue syndrome. Neuroreport. 2004 Dec 3;15(17):2571-2574. Yamamoto, Shigeyuki [*]; Ouchi, Yasuomi [1]; Onoe, Hirotaka [2]; Yoshikawa, Etsuji [3]; Tsukada, Hideo [3]; Takahashi, Hidetoshi [4]; Iwase, Masao [4]; Yamaguti, Kouzi [5]; Kuratsune, Hirohiko[5, 6]; Watanabe, Yasuyoshi [*,CA] Affiliations: [*] Department of Physiology, Osaka City University Graduate School of Medicine, 1-4-3 Asahimachi, Abeno-ku, Osaka 545-8585 [1] Positron Medical Center, Hamamatsu Medical Center, 5000 Hirakuchi, Hamakita, Shizuoka 434-0041 [2] Department of Psychology, Tokyo Metropolitan Institute for Neuroscience, 2-6 Musashidai Fuchu, Tokyo 183-8526 [3] Central Research Laboratory, Hamamatsu Photonics KK, 5000 Hirakuchi, Hamakita, Shizuoka 434-8601 [4] Psychiatry, Department of Clinical Neuroscience [5] Department of Hematology and Oncology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita 565-0871 [6] Department of Health Sciences, Faculty of Health Sciences for Welfare, Kansai University of Welfare Sciences, 3-11-1 Asahigaoka, Kashiwara 582-0026, Japan [CA] Corresponding Author: yywata@med.osaka-cu.ac.jp Received 10 September 2004; accepted 6 October 2004 NLM Citation: PMID: 15570154 To assess the involvement of serotonin in the symptoms of chronic fatigue syndrome, we investigated the serotonergic neurotransmitter system of chronic fatigue syndrome patients by the positron emission tomography (PET). Here we show that the density of serotonin transporters (5-HTTs) in the brain, as determined by using a radiotracer, [C](+)McN5652, was significantly reduced in the rostral subdivision of the anterior cingulate as compared with that in normal volunteers. This subdivision is different from that in the dorsal anterior cingulate in which binding potential values of individual patient showed a weak negative correlation with self-reported pain score of the patients. Therefore, an alteration of serotonergic system in the rostral anterior cingulate plays a key role in pathophysiology of chronic fatigue syndrome.