scholarly journals Distribution across tissue layers of extrinsic nerves innervating the mouse colorectum - Anin vitroanterograde tracing study

2014 ◽  
Vol 26 (10) ◽  
pp. 1494-1507 ◽  
Author(s):  
Pablo R. Brumovsky ◽  
Jun-Ho La ◽  
Gerald F. Gebhart
Keyword(s):  
Extrinsic Nerves

Pancreatic bicarbonate response to HCl before and after cutting the extrinsic nerves of the pancreas in dogs

1988 ◽  
Vol 254 (3) ◽  
pp. G436-G443
Author(s):  
W. Niebel ◽  
C. Beglinger ◽  
M. V. Singer
Keyword(s):  
Surgical Procedures ◽  
Plasma Levels ◽  
Truncal Vagotomy ◽  
Vagus Nerves ◽  
Splanchnic Nerves ◽  
Before And After ◽  
Pancreatic Fistulas ◽  
Bicarbonate Output ◽  
Intravenous Atropine ◽  
Extrinsic Nerves

In two sets of dogs with gastric and pancreatic fistulas, we studied the effect of atropine on pancreatic bicarbonate output and release of secretin in response to intraduodenal HCl before and after stepwise removal of the extrinsic nerves of the pancreas, i.e., celiac and superior mesenteric ganglionectomy alone or truncal vagotomy alone and truncal vagotomy plus celiac and superior mesenteric ganglionectomy. Ganglionectomy alone did not alter the incremental bicarbonate response to HCl. Truncal vagotomy alone significantly (P less than 0.05) decreased the incremental bicarbonate response to low (1.5 and 3 mmol/h) but not high (6 to 24 mmol/h) loads of HCl. Additional ganglionectomy restored the bicarbonate response to prevagotomy levels. With the extrinsic nerves intact and after ganglionectomy, but not after truncal vagotomy and truncal vagotomy plus ganglionectomy, intravenous atropine (14 nmol.kg-1.h-1) significantly reduced the incremental bicarbonate response to low (1.5 and 3 mmol/h) but not high loads of HCl. Neither the different surgical procedures nor atropine significantly altered plasma levels of secretin basally and in response to intestinal HCl. We conclude that 1) cholinergic fibers within the vagus nerves but not the splanchnic nerves are important mediators of the pancreatic bicarbonate response to low loads of HCl and 2) release of secretin by intestinal HCl is not under cholinergic and splanchnic control.

Extrinsic nerves of the chicken's uterus (shell gland)

1963 ◽  
Vol 147 (3) ◽  
pp. 431-437 ◽  
Author(s):  
S. L. Freedman ◽  
P. D. Sturkie
Keyword(s):  
Shell Gland ◽  
Extrinsic Nerves

Cholinergic control of canine antral immunoreactive gastrin release and motility

1982 ◽  
Vol 60 (7) ◽  
pp. 893-901 ◽  
Author(s):  
J. E. T. Fox ◽  
E. E. Daniel ◽  
J. Jury ◽  
N. S. Track ◽  
S. Chiu
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Muscarinic Receptor ◽  
Muscle Cell ◽  
Gastrin Release ◽  
Field Stimulation ◽  
Antral Motility ◽  
Stimulation Of ◽  
Extrinsic Nerves

We used acute anaesthetized dogs to investigate the role of cholinergic receptors in the relationship between antral immunoreactive (I) gastrin release and antral motility. Electrical stimulation of extrinsic nerves via the cervical vagus or the nerve of Latarjet appeared to increase I gastrin release and antral motility by separate pathways as blockade of muscarinic receptors, i.e., atropinization inhibited motility but did not alter I gastrin release. On the other hand, blockade of nicotinic receptors by hexamethonium treatment obliterated I gastrin release induced by stimulation of the extrinsic nerves but only reduced motility. Field stimulation of intrinsic nerves via serosal electrodes also increased both I gastrin release and local motility. Since hexamethonium treatment only slightly reduced both I gastrin release and motility and atropinization eliminated both during field stimulation, the presence of a muscarinic receptor in the final pathway for each is proposed.Atropine eliminated carhachol-induced I gastrin release and motility increases, even in the presence of nerve blockade by tetrodotoxin. This suggests that this muscarinic receptor is on the smooth muscle cell itself and possibly on the gastrin cell. However a proposed role of the somatostatin cell in controlling gastrin release is also consistent with these data.Thus, both an intrinsic cholinergic and a separate extrinsic noncholinergic pathway are involved in antral release of I gastrin but initiation of motility appears to involve a final common pathway terminating in a muscarinic receptor on the smooth muscle cell.

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