PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 18817806-0 2009 Intracerebroventricular fluvoxamine administration inhibited pain behavior but increased Fos expression in affective pain pathways. Fluvoxamine 24-35 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 89-92 18817806-7 2009 Moreover, fluvoxamine alone increased Fos in the BL and PFC. Fluvoxamine 10-21 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 38-41 18817806-9 2009 The results indicated that 5-HT2 receptor activities participate minimally in Fos induction by fluvoxamine in the PFC and BL. Fluvoxamine 95-106 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 78-81 18817806-10 2009 In contrast, WAY-100635 affected the Fos expression produced by fluvoxamine. Fluvoxamine 64-75 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 37-40 18817806-11 2009 In the portion of the brain with affectional pain pathways, 5-HT1 receptor activities induced anti-nociceptive effects and decreased Fos expression with fluvoxamine, while 5-HT2 receptor activation affected to anti-nociceptive effects but did not induce Fos expression. Fluvoxamine 153-164 Fos proto-oncogene, AP-1 transcription factor subunit Homo sapiens 133-136