An ultrastructural evidence for the expression of transient receptor potential ankyrin 1 (TRPA1) in astrocytes in the rat trigeminal caudal nucleus

► TRPA1 immunoreactivity was observed in the astrocyte in the superficial lamina of the trigeminal caudal nucleus. ► TRPA1 expression was increased in the process of the astrocyte following TMJ inflammation. ► These findings suggest an existence of novel pathway of TRPA1 involvement in the central m...

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Bibliographic Details
Published in:Journal of chemical neuroanatomy 2012-10, Vol.45 (1-2), p.45-49
Main Authors: Lee, Sang Man, Cho, Yi Sul, Kim, Tae Heon, Jin, Myoung Uk, Ahn, Dong Kuk, Noguchi, Koichi, Bae, Yong Chul
Format: Article
Language:English
Subjects:
Anatomy
Animals
Ankyrin
Astrocyte
Astrocytes
Astrocytes - metabolism
Astrocytes - ultrastructure
Brain architecture
Brain stem
Immunohistochemistry
Immunoreactivity
Inflammation
Injuries
Male
Microscopy, Electron, Transmission
Nerves
Pain perception
Rats
Rats, Sprague-Dawley
Sensory neurons
Temporomandibular joint
transient receptor potential proteins
Trigeminal
Trigeminal Caudal Nucleus - metabolism
Trigeminal Caudal Nucleus - ultrastructure
TRPA1
TRPA1 Cation Channel
TRPC Cation Channels - biosynthesis
Ultrastructure
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Summary:► TRPA1 immunoreactivity was observed in the astrocyte in the superficial lamina of the trigeminal caudal nucleus. ► TRPA1 expression was increased in the process of the astrocyte following TMJ inflammation. ► These findings suggest an existence of novel pathway of TRPA1 involvement in the central mechanisms of inflammatory hyperalgesia. The transient receptor potential ankyrin 1 (TRPA1) is implicated in the mechanical and cold hyperalgesia following inflammation and nerve injury. Its expression has been presumed to be confined to primary afferent terminals. Here, we show that TRPA1 is expressed in astrocytes in the superficial laminae of the rat trigeminal caudal nucleus by use of electron microscopic immunoperoxidase and immunogold labeling techniques. Immunoreactivity for TRPA1 was consistently observed in somata and process of astrocytes and was weaker than that in presumed nociceptive primary afferent terminals, but increased significantly in the fine process of astrocyte in rats with experimental inflammation of the temporomandibular joint. Thus, we provide ultrastructural evidence that TRPA1 is expressed in astrocytes in the brain stem and propose a novel pathway of its involvement in the central mechanism of inflammatory hyperalgesia.
ISSN:0891-0618
1873-6300
DOI:10.1016/j.jchemneu.2012.07.003