Effect of Brn-3a deficiency on parvalbumin-, calbindin D-28k-, calretinin- and calcitonin gene-related peptide-immunoreactive primary sensory neurons in the trigeminal ganglion

H. Ichikawa, T. Yamaai, D. M. Jacobowitz, Z. Mo, M. Xiang, T. Sugimoto

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

Immunohistochemistry for parvalbumin, calbindin D-28k, calretinin and calcitonin gene-related peptide (CGRP) was performed on the trigeminal ganglion and oro-facial tissues in Brn-3a wildtype and knockout mice at embryonic day 18.5 and postnatal day 0. In wildtype mice, the trigeminal ganglion contained abundant parvalbumin-, calbindin D-28k- and CGRP-immunoreactive neurons while the ganglion was almost devoid of calretinin-immunoreactive neurons. In Brn-3a knockout mice, a 63% decrease of parvalbumin-immunoreactive neurons was detected. In contrast, the absence of Brn-3a dramatically increased the number of calbindin D-28k-immunoreactive (3.5-fold increase) and calretinin-immunoreactive neurons (91-fold increase). The number of CGRP-immunoreactive neurons, however, was not altered by the Brn-3a deficiency. Cell size analysis indicated that loss of Brn-3a increased the proportions of small (2) parvalbumin-, calbindin D-28k- and CGRP-immunoreactive neurons while it decreased those of large (>200 μm2) immunoreactive cells. Calretinin-immunoreactive neurons were either small or medium (100-200 μm2) in mutant mice. The oro-facial tissues contained parvalbumin-, calbindin D-28k- and CGRP-immunoreactive fibers, but not calretinin-immunoreactive ones in wildtype mice. In Brn-3a knockout mice, the number of parvalbumin-immunoreactive fibers markedly decreased in the infraorbital nerve and parvalbumin-immunoreactive endings disappeared in the vibrissa. In contrast, the number of calbindin D-28k-immunoreactive fibers increased significantly in the infraorbital and mental nerves. In addition, calbindin D-28k-immunoreactive endings appeared in the vibrissa. As well, some fibers showed calretinin-immunoreactivity in the infraorbital nerve of the mutant. However, no obvious change of CGRP-immunoreactive fibers was observed in the oro-facial region of knockout mice. Taken together, our data suggest that Brn-3a deficiency has effects on the expression of neurochemical substances in the trigeminal ganglion.

Original languageEnglish
Pages (from-to)537-546
Number of pages10
JournalNeuroscience
Volume113
Issue number3
DOIs
Publication statusPublished - Sep 2 2002

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Calbindin 2
Calbindins
Parvalbumins
Trigeminal Ganglion
Calcitonin Gene-Related Peptide
Sensory Receptor Cells
Neurons
Knockout Mice
Vibrissae
Cell Size
Ganglia
Immunohistochemistry

Keywords

  • Immunohistochemistry
  • Knockout mouse
  • Neurochemical substances
  • Primary sensory neurons
  • Transcription factor

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Effect of Brn-3a deficiency on parvalbumin-, calbindin D-28k-, calretinin- and calcitonin gene-related peptide-immunoreactive primary sensory neurons in the trigeminal ganglion. / Ichikawa, H.; Yamaai, T.; Jacobowitz, D. M.; Mo, Z.; Xiang, M.; Sugimoto, T.

In: Neuroscience, Vol. 113, No. 3, 02.09.2002, p. 537-546.

Research output: Contribution to journalArticle

Ichikawa, H. ; Yamaai, T. ; Jacobowitz, D. M. ; Mo, Z. ; Xiang, M. ; Sugimoto, T. / Effect of Brn-3a deficiency on parvalbumin-, calbindin D-28k-, calretinin- and calcitonin gene-related peptide-immunoreactive primary sensory neurons in the trigeminal ganglion. In: Neuroscience. 2002 ; Vol. 113, No. 3. pp. 537-546.
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abstract = "Immunohistochemistry for parvalbumin, calbindin D-28k, calretinin and calcitonin gene-related peptide (CGRP) was performed on the trigeminal ganglion and oro-facial tissues in Brn-3a wildtype and knockout mice at embryonic day 18.5 and postnatal day 0. In wildtype mice, the trigeminal ganglion contained abundant parvalbumin-, calbindin D-28k- and CGRP-immunoreactive neurons while the ganglion was almost devoid of calretinin-immunoreactive neurons. In Brn-3a knockout mice, a 63{\%} decrease of parvalbumin-immunoreactive neurons was detected. In contrast, the absence of Brn-3a dramatically increased the number of calbindin D-28k-immunoreactive (3.5-fold increase) and calretinin-immunoreactive neurons (91-fold increase). The number of CGRP-immunoreactive neurons, however, was not altered by the Brn-3a deficiency. Cell size analysis indicated that loss of Brn-3a increased the proportions of small (2) parvalbumin-, calbindin D-28k- and CGRP-immunoreactive neurons while it decreased those of large (>200 μm2) immunoreactive cells. Calretinin-immunoreactive neurons were either small or medium (100-200 μm2) in mutant mice. The oro-facial tissues contained parvalbumin-, calbindin D-28k- and CGRP-immunoreactive fibers, but not calretinin-immunoreactive ones in wildtype mice. In Brn-3a knockout mice, the number of parvalbumin-immunoreactive fibers markedly decreased in the infraorbital nerve and parvalbumin-immunoreactive endings disappeared in the vibrissa. In contrast, the number of calbindin D-28k-immunoreactive fibers increased significantly in the infraorbital and mental nerves. In addition, calbindin D-28k-immunoreactive endings appeared in the vibrissa. As well, some fibers showed calretinin-immunoreactivity in the infraorbital nerve of the mutant. However, no obvious change of CGRP-immunoreactive fibers was observed in the oro-facial region of knockout mice. Taken together, our data suggest that Brn-3a deficiency has effects on the expression of neurochemical substances in the trigeminal ganglion.",
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AU - Yamaai, T.

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AU - Xiang, M.

AU - Sugimoto, T.

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KW - Transcription factor

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