title: Effect of Brn-3a deficiency on primary nociceptors in the trigeminal ganglion.
abstract: Immunohistochemistry for substance P, somatostatin and vanilloid receptor subtype 1 as well as receptors for somatostatin and opioids was performed on the trigeminal ganglion in wild-type and Brn-3a knockout mice at postnatal day 0. In wild-type mice, the trigeminal ganglion contained abundant substance P-, vanilloid receptor subtype 1-, sst2A receptor- and delta-opioid receptor-immunoreactive neurons, while the ganglion had only a few mu-opioid receptor-immunoreactive neurons. The Brn-3a deficiency had an effect on the cell size but not the number of substance P-immunoreactive neurons. In knockout mice, the proportion of small immunoreactive neurons markedly increased and that of medium- to large-sized immunoreactive ones correspondingly decreased (mean +/- S.D. = 54.7 +/- 29.1 microm2, range = 10.9-220.8 microm2) compared to wild-type mice (mean +/- S.D. = 116.6 +/- 58.6 microm2, range = 27.3-400.7 microm2). As for vanilloid receptor subtype 1-immunoreactive neurons, the number and cell size was barely affected by the deficiency. On the other hand, the loss of Brn-3a caused a decrease in the number of sst2A receptor- or delta-opioid receptor-immunoreactive neurons (more than 95% reduction) and an increase in the number of mu-opioid receptor-immunoreactive neurons (9.3-fold increase). Somatostatin-immunoreactive neurons were not detected in the trigeminal ganglion of wild-type or mutant mice at postnatal day 0. The present study suggests that Brn-3a deficiency may have effects on the survival of trigeminal nociceptors and their expression of some neurochemical substances.
authors.affiliation: Department of Oral Function and Anatomy, Okayama University Graduate School of Medicine and Dentistry, Okayama 700-8525, Japan. hiroichi@md.okayama-u.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Ichikawa
authors.forename: S
authors.initials: S
authors.lastname: Schulz
authors.forename: V
authors.initials: V
authors.lastname: Höllt
authors.forename: Z
authors.initials: Z
authors.lastname: Mo
authors.forename: M
authors.initials: M
authors.lastname: Xiang
authors.forename: T
authors.initials: T
authors.lastname: Sugimoto
mesh_terms: D000818:Animals; D002452:Cell Count; D048429:Cell Size; D004268:DNA-Binding Proteins / Q000172:deficiency*; D007150:Immunohistochemistry; D051379:Mice; D018345:Mice, Knockout; D009474:Neurons / Q000378:metabolism*; D009619:Nociceptors / Q000378:metabolism*; D011955:Receptors, Drug / Q000378:metabolism; D018040:Receptors, Neurokinin-1 / Q000378:metabolism; D011957:Receptors, Opioid / Q000378:metabolism; D017481:Receptors, Somatostatin / Q000378:metabolism; D050916:TRPV Cation Channels; D050818:Transcription Factor Brn-3; D050819:Transcription Factor Brn-3A; D014157:Transcription Factors / Q000172:deficiency*; D012668:Trigeminal Ganglion / Q000378:metabolism*
chemical_list: D004268:DNA-Binding Proteins; C494189:Pou4f1 protein, mouse; D011955:Receptors, Drug; D018040:Receptors, Neurokinin-1; D011957:Receptors, Opioid; D017481:Receptors, Somatostatin; D050916:TRPV Cation Channels; C494484:TRPV1 receptor; D050818:Transcription Factor Brn-3; D050819:Transcription Factor Brn-3A; D014157:Transcription Factors