Effect of Brn-3a deficiency on primary nociceptors in the trigeminal ganglion

H. Ichikawa, S. Schulz, V. Höllt, Z. Mo, M. Xiang, T. Sugimoto

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9 Citations (Scopus)


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 μm2, range = 10.9-220.8 μm2) compared to wild-type mice (mean ± S.D. = 116.6 ± 58.6 μm2, range = 27.3-400.7 μm2). 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.

Original languageEnglish
Pages (from-to)445-451
Number of pages7
JournalNeuroscience Research
Issue number4
Publication statusPublished - Apr 2005


  • Capsaicin receptor
  • Immunohistochemistry
  • Knockout mouse
  • Neuropeptides
  • Transcription factor
  • Trigeminal ganglion

ASJC Scopus subject areas

  • Neuroscience(all)


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