scholarly journals Direct Evidence for Central Action of PCPGABA to Stimulate Gastric Acid Secretion by Intracisternal Injection

1990 ◽  
Vol 54 (1) ◽  
pp. 7-12 ◽  
Author(s):  
Katsuya YAMASAKI ◽  
Yoshiaki GOTO
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Direct Evidence ◽  
Central Action ◽  
Intracisternal Injection

Intracisternal injection of TRH precursor, TRH-glycine, stimulates gastric acid secretion in rats

1989 ◽  
Vol 25 (1) ◽  
pp. 51-60 ◽  
Author(s):  
R.L. Stephens ◽  
A.E. Pekary ◽  
J.J. DiStephano ◽  
E. Landaw ◽  
Y. Taché
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Intracisternal Injection

scholarly journals Peripheral PYY inhibits intracisternal TRH-induced gastric acid secretion by acting in the brain

2000 ◽  
Vol 279 (3) ◽  
pp. G575-G581 ◽  
Author(s):  
Hong Yang ◽  
Keishi Kawakubo ◽  
Helen Wong ◽  
Gordon Ohning ◽  
John Walsh ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Peptide Yy ◽  
Vagal Stimulation ◽  
Inhibitory Effect ◽  
Supporting Evidence ◽  
Intracisternal Injection ◽  
Site Of Action ◽  
The Brain

The site of action of peripheral peptide YY (PYY)-induced inhibition of vagally stimulated gastric acid secretion was studied using immunoneutralization with PYY antibody in urethan-anesthetized rats. Gastric acid secretion (59 ± 7 μmol/90 min) stimulated by intracisternal injection of the stable thyrotropin-releasing hormone (TRH) analog RX-77368 (14 pmol/rat) was dose-dependently inhibited by 52%, 69%, and 83% by intravenous infusion of 0.25, 0.5, and 1.0 nmol · kg−1 · h−1 PYY, respectively. PYY or PYY3–36 (2.4 pmol/rat) injected intracisternally also inhibited the acid response to intracisternal RX-77368 by 73% and 80%, respectively. Intravenous pretreatment with PYY antibody (4.5 mg/rat), which shows a 35% cross-reaction with PYY3–36 by RIA, completely prevented the inhibitory effect of intravenously infused PYY (1 nmol · kg−1 · h−1). When injected intracisternally, the PYY antibody (280 μg/rat) reversed intracisternal PYY (2.4 pmol)- and intravenous PYY (1 nmol · kg−1 · h−1)-induced inhibition of acid response to intracisternal RX-77368 by 64% and 93.5%, respectively. These results provide supporting evidence that peripheral PYY inhibits central vagal stimulation of gastric acid secretion through an action in the brain.

Apolipoprotein A-IV acts in the brain to inhibit gastric emptying in the rat

1996 ◽  
Vol 270 (1) ◽  
pp. G49-G53 ◽  
Author(s):  
T. Okumura ◽  
K. Fukagawa ◽  
P. Tso ◽  
I. L. Taylor ◽  
T. N. Pappas
Keyword(s):  
Gastric Emptying ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Intraperitoneal Administration ◽  
Phenol Red ◽  
Dependent Manner ◽  
Liquid Meal ◽  
Apolipoprotein A ◽  
Intracisternal Injection

We have very recently shown that intracisternal injection of apolipoprotein A-IV (apo A-IV), a glycoprotein produced in the small intestine by fat, dose-dependently inhibited gastric acid secretion in pylorus-ligated conscious rats. These results suggest that apo A-IV acts centrally as a neuromodulator to inhibit gastric secretion. The present study was carried out to examine the hypothesis that apo A-IV acts centrally to alter gastric emptying. Rats fasted 24 h received intracisternal injection of apo A-IV and a liquid meal by oral intubation under brief isoflurane anesthesia. Gastric emptying of a liquid meal was determined by the phenol red method. Intracisternal injection of apo A-IV inhibited gastric emptying of a liquid meal in a dose-dependent manner (1.0-4.0 micrograms). On the other hand, apo A-I in a dose of 4 micrograms failed to change gastric emptying. Gastric emptying was not altered by intraperitoneal administration of apo A-IV in a dose of 15 micrograms. These results suggest that apo A-IV acts centrally to delay gastric emptying of a liquid meal. Together with our recent finding that apo A-IV acts centrally to inhibit gastric acid secretion, the present study supports our hypothesis that apo A-IV may be involved in lipid-induced inhibition of gastric function.

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