1.Vanilloid Receptor Type-1 Immunoreactivities in the Mouse Myenteric Plexus: Immunohistochemical and Electrophysiological Study.
Jae Yeoul JUN ; En Seok YANG ; Kee Hune KIM ; In Youb CHANG
Korean Journal of Physical Anthropology 2004;17(1):45-53
The vanilloid receptor type-1 (VR1) is a nonselective cation channel activated by capsaicin and can be act as mediator of chemical and physical stimuli that elicit pain. The presence of VR1 in the dorsal root, trigeminal and nodose ganglia has been firmly established, but it unclear in the mouse intestinal wall. The distribution of VR1 receptors in mouse afferent neurons innervating the intestinal tract was investigated by immunohistochemistry. Also small and large intestines were dual-labelled with antibody for VR1 and marker for interstitial cells of Cajal (c-kit). VR1-immunopositive cells were localized on fine fibers in myenteric plexus and expressed weakly myenteric ganglia. The majority of VR1-immunopositive fibers are not colocalized with or apposed to c-kit positive interstitial cells of Cajal. Also electrophysiologically capsaicin had no effect on cultured interstitial cells of Cajal. It is concluded that VR1-immunoreactive intestinal nerves are mainly distributed in myenteric plexus of murine intestinal wall, and vanillod may be not directly related to interstitial cells of Cajal in regulation of intestinal motility.
Animals
;
Capsaicin
;
Ganglia
;
Gastrointestinal Motility
;
Immunohistochemistry
;
Interstitial Cells of Cajal
;
Intestines
;
Mice*
;
Myenteric Plexus*
;
Neurons, Afferent
;
Nodose Ganglion
;
Spinal Nerve Roots
2.Vanilloid Receptor Type-1 Immunoreactivities in the Mouse Myenteric Plexus: Immunohistochemical and Electrophysiological Study.
Jae Yeoul JUN ; En Seok YANG ; Kee Hune KIM ; In Youb CHANG
Korean Journal of Physical Anthropology 2004;17(1):45-53
The vanilloid receptor type-1 (VR1) is a nonselective cation channel activated by capsaicin and can be act as mediator of chemical and physical stimuli that elicit pain. The presence of VR1 in the dorsal root, trigeminal and nodose ganglia has been firmly established, but it unclear in the mouse intestinal wall. The distribution of VR1 receptors in mouse afferent neurons innervating the intestinal tract was investigated by immunohistochemistry. Also small and large intestines were dual-labelled with antibody for VR1 and marker for interstitial cells of Cajal (c-kit). VR1-immunopositive cells were localized on fine fibers in myenteric plexus and expressed weakly myenteric ganglia. The majority of VR1-immunopositive fibers are not colocalized with or apposed to c-kit positive interstitial cells of Cajal. Also electrophysiologically capsaicin had no effect on cultured interstitial cells of Cajal. It is concluded that VR1-immunoreactive intestinal nerves are mainly distributed in myenteric plexus of murine intestinal wall, and vanillod may be not directly related to interstitial cells of Cajal in regulation of intestinal motility.
Animals
;
Capsaicin
;
Ganglia
;
Gastrointestinal Motility
;
Immunohistochemistry
;
Interstitial Cells of Cajal
;
Intestines
;
Mice*
;
Myenteric Plexus*
;
Neurons, Afferent
;
Nodose Ganglion
;
Spinal Nerve Roots
3.Change of Interstitial Cells of Cajal (ICC) and Intestinal Motility in Murine Small Bowel Obstruction.
Jae Yeoul JUN ; Choon Hae CHUNG ; Ho Jin YOU ; Kyung Hee KIM ; Jang Man KIM ; Kee Hune KIM ; Do Young PARK ; In Youb CHANG
Korean Journal of Anatomy 2002;35(5):387-396
Interstitial cells of Cajal (ICC) are the pacemakers in gastrointestinal slow wave, and also transduce signal inputs from the enteric nervous system to smooth muscle. The abnormal motility corresponded to a lack or decreasing of ICC and a disruption of electrical slow waves. So we developed partial obstruction model in murine small intestine and investigated changes in the ICC networks and electrical activity in the obstructed bowel using c-kit immunohistochemistry and intracelluar electrophysiological techniques. Two weeks following the onset of a partial obstruction, the small intestine increased in diameter and muscular hypertrophy was developed oral to the obstruction site. ICC were absent or only weak at 1 ~25 mm oral to the occlusion site, and this disruption was accompanied by the loss of electrical slow wave. ICC networks and slow waves were normal appearance aboral to the clip. In conclusion, The present results showed that partial intestinal obstruction induced the loss of ICC networks and slow waves. These result will provide a valuable aid for understanding pathogenesis of intestinal motility disorder, and this model may be an important tool for evaluating genetic or molecular factor for the therapeutic opportunities of motility disorder in human.
Animals
;
Enteric Nervous System
;
Gastrointestinal Motility*
;
Humans
;
Hypertrophy
;
Immunohistochemistry
;
Interstitial Cells of Cajal*
;
Intestinal Obstruction
;
Intestine, Small
;
Mice
;
Muscle, Smooth