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HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY II 



as sali\ation, nose licking or swallowing, were ob- 

 served in these experiments. Bilateral \agotomy did 

 not abolish the response. Wang & Borison (93) 

 reported in 1950 a series of experiments on dogs in 

 which the region responsive to stimulation was de- 

 stroyed; following this the animals showed a pro- 

 nounced refractoriness to chemicalK -induced vomit- 

 ing. There was still a definite response to intragastric 

 administration of large doses of copper sulfate 

 which, however, might have been due to a generalized 

 toxic action. It is conceivable that if a sufficient dose of 

 an emetic agent is given, the direct action of the drug 

 on the various substations of the reflex may be suffi- 

 cient to induce vomiting. In spite of frequent stimu- 

 lation of other regions of cat and dog brains, no report 

 has been published in which true vomiting has been 

 reported to occur on electrical stimulation or ablation 

 of any other structure of the brain. X'omiting has not 

 been seen by Penfield's group in their extensive ex- 

 ploration of the cortical surface of man (72). It does 

 appear that irrespective of the afferent impulse lead- 

 ing to vomiting the complex process has to be in- 

 tegrated through a medullary structure, presumably 

 the one described by Wang & Borison {93). 



G.-^STRIC SECRETION 



Psychic secretion of gastric juice depends on the 

 integrity of the cerebral cortex, as pointed out by 

 Pavlov (70). He received support in this assumption 

 through the experiments of Guerver (41 ) who showed 

 that stimulation of an area just outside the forward 

 end of the sigmoid gyrus in dogs produced a copious 

 flow of gastric secretion. This secretion consisted 

 initially of a highly mucoid juice followed by hydro- 

 chloric acid and pepsin. The secretion was dependent 

 on the integrity of the vagus ner\es. Greker (40) 

 ablated this area and found that a marked diminution 

 in gastric secretion occurred over a period of 7 to 8 

 days after which the secretory values returned to 

 normal. Many years later Watts & Fulton (94) 

 observed, in studying the relationship of the cerebral 

 cortex to gastrointestinal motility, that some of the 

 stimulated animals at necropsy showed a considerable 

 amount of secretion in the stomach. They drew the 

 conclusion that the stimuli affecting tlie gastroin- 

 testinal motility also affected gastric secretion. 

 Their observations were repeated by Davey el al. 

 (22) who explored the possibility of eliciting gastric 

 secretion by stimulating the frontal lobe in dogs and 

 monkeys. The experimental difficulties in the collec- 



tion of gastric juice are considerable because we must 

 assume that the operative procedures including the 

 insertion of a cannula must necessarily influence the 

 local state of the gastric glands. It has also been clearly 

 shown that some of the anesthetics used in themselves 

 influence the amount of secretion even w hen given in 

 very small amounts (80). Davey and his associates 

 (22) found an area in the frontal lobe of the dog and 

 monkey which was roughly the same as the one earlier 

 found by Guerver and in which stimuli of long dura- 

 tion and fairlv high frequencies activated the gastric 

 glands. The hydrochloric acid secretion turned out 

 to be dependent on the state of anesthesia, but pepsin 

 and inucus secretions could be increased two to four 

 times by stimulation of this area Injury to the area 

 resulted in diminished response. In a discussion fol- 

 lowing the presentation of this work Davey indicated 

 that a possible pathway would be via the lenticular 

 nucleus, portions of the thalamus and the quadri- 

 geminal bodies. This was on the basis of earlier re- 

 ported experiments and no attempts were made to 

 confirm this idea. 



In order to facilitate the recording of the gastric 

 acidity changes, Klopper (52) developed a method for 

 continuous registration of gastric pH through elec- 

 trodes introduced through the esophagus. These ex- 

 periments showed that, on stimulation of an area 

 just inferior to the anterior sigmoid gyrus in the cat 

 with an optimal frequency of 15 impulses per sec. 

 and a duration of 10 to 15 msec, a definite decrease 

 in gastric pH was obtained. The area defined was the 

 same as that found by Eliasson in 1952 for gastric 

 motor function. Klopper also found that electrical 

 stimulation of this area inhibited gastric motility 

 which might be one reason that the duodenal secre- 

 tion did not influence the gastric pH. No other por- 

 tion of the cerebral cortex was found to influence 

 gastric secretion on stimulation. The secretion of gas- 

 tric juice continued up to 20 min. after the end of the 

 stimulation This indicated to Klopper that possibly 

 the efTect of the cortical stimulation could be a re- 

 lease of a hormone, such as gastrin, or of histamine 

 leading to a secondary .secretion from the gastric 

 mucosa. 



Subcortical areas ha\c long been known to react 

 to stimulation ijy increasing the gastric acidity. 

 Heslop (44) and Sheehan (84) demonstrated in con- 

 nection with a study of gastric movements a definite 

 increase in gastric acidity. Jogi et al. (49) observed 

 that the secretory response to insulin-induced hypo- 

 glycemia disappears after decerebration but remains 

 unchanged after decortication. Porter et al. (75) 



