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ID 111345
Author
Matsushima, Ayumi Okayama University
Ichikawa, Hiroyuki Tohoku University
Fujita, Masako Okayama University
Mitoh, Yoshihiro Okayama University
Kobashi, Motoi Okayama University
Yamashiro, Takashi Okayama University
Matsuo, Ryuji Okayama University
Keywords
superior salivatory nucleus
immunohistochemistry
GABAergic neuron
FluoroGold
Content Type
Journal Article
Description
The superior salivatory nucleus (SSN) is the primary parasympathetic center controlling submandibular salivatory secretion. Our previous electrophysiological study revealed that many SSN neurons receive GABAergic and glycinergic synaptic inputs. In the present study, we examined the distribution of GABAergic and glycinergic nerve terminals, GABAA receptors in the SSN, and the origin of GABAergic nerve terminals innervating the SSN. Glutamic acid decarboxylase (GAD) and glycine transporter 2 (GLYT2) were used as markers of GABAergic and glycinergic nerve terminals, respectively. GAD- and GLYT2-positive nerve terminals and GABAA receptors were examined immunohistochemically in SSN neurons labeled by the retrograde axonal transport of FastBlue (FB) injected into the chorda-lingual nerve. The SSN neurons abundantly contained GAD-positive nerve terminals and GABAA receptors, suggesting that SSN neurons undergo strong GABAergic inhibition. The origin of GABAergic terminals was examined in neurons labeled by the retrograde transport of FluoroGold (FG) injected into the SSN. GAD was used as a marker of GABAergic neurons. Numerous FG-labeled neurons were found in the forebrain and brainstem. However, in FG-labeled neurons, GAD-positive neurons were occasionally observed in the reticular formation of the brainstem. These findings suggest that SSN neurons mainly receive GABAergic projections from the reticular formation.
Journal Title
The Journal of Medical Investigation
ISSN
13496867
13431420
NCID
AA11166929
AA12022913
Publisher
Faculty of Medicine Tokushima University
Volume
56
Issue
Supplement
Start Page
264
End Page
266
Sort Key
264
Published Date
2009-12
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Publisher