Effects of extrinsic autonomic inputs on expression of c-Fos immunoreactivity in myenteric neurons of the guinea pig distal colon.
c-Fos protein is a nuclear protein coded by c-fos proto-oncogene subsequent to synaptic activation of the neurons. We used immunohistochemical methods to visualize the expression of c-Fos protein in myenteric neurons of the guinea pig distal colon and examined the effects of the extrinsic autonomic inputs on the enteric circuits. No c-Fos immunoreactivity was observed in the colonic segments fixed immediately after removal from the animal body. A number of c-Fos-immunoreactive nuclei of myenteric neurons, however, appeared in all preparations that were incubated in Krebs solution in vitro (n=10). Application of tetrodotoxin (0.2 microM) abolished the expression of c-Fos-immunoreactivity (n=6), but hexamethonium (100 microM) failed to decrease the number of c-Fos-positive neurons despite a complete suppression of spontaneous peristaltic movements (n=5). Neither the electrical stimulation (n=8) nor the severing of the pelvic nerves (n=5) changed the number of c-Fos-positive neurons. Application of clonidine, an alpha(2)-agonist, (0.1 microM) abolished the expression of c-Fos protein in all preparations (n=5), while denervation of the sympathetic fibers in the lumbar colonic and hypogastric nerves in vivo increased the number of c-Fos-positive neurons (n=5). The results indicate that the enteric circuit in the distal part of the gastrointestinal tract is under tonic inhibition by the sympathetic nervous system from the lumbar spinal cord. c-Fos immunoreactivity expressed in the colonic preparations in vivo might be the results of enhanced activation of non-nicotinic receptors after removal of the sympathetic inhibition.
Yuyama
Noriyuki
N
Department of Oral Physiology, Kanagawa Dental College, 82 Inaoka-cho, Yokosuka 238-8580, Japan.
Mizuno
Junzo
J
Tsuzuki
Hideko
H
Wada-Takahashi
Satoko
S
Takahashi
Osamu
O
Tamura
Kenji
K
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D017776:Autonomic Pathways / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D002452:Cell Count; D002467:Cell Nucleus / Q000378:metabolism; D003000:Clonidine / Q000494:pharmacology; D003106:Colon / Q000294:innervation* / Q000378:metabolism; D004558:Electric Stimulation; D005730:Ganglionic Blockers / Q000494:pharmacology; D006168:Guinea Pigs; D018738:Hexamethonium / Q000494:pharmacology; D007150:Immunohistochemistry; D008297:Male; D009197:Myenteric Plexus / Q000166:cytology*; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D010528:Peristalsis / Q000187:drug effects / Q000502:physiology; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis*; D013562:Sympathectomy; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology
D000316:Adrenergic alpha-Agonists; D005730:Ganglionic Blockers; D016760:Proto-Oncogene Proteins c-fos; D018738:Hexamethonium; D013779:Tetrodotoxin; D003000:Clonidine