REGULATION OF FOOD AND WATER INTAKE 359 



fluid or as a food depending upon whether they are thirsty or hungry. 

 Lateral hypothalamic animals seem to lack the capacity to detect true thirst. 

 They eat the saccharine ; they do not drink it. 



Finally, a fourth stage ensues in the recovery from lateral hypothalamic 

 lesions. Most animals with small lateral hypothalamic lesions eventually 

 begin to drink water and are able to eat sufficient food to maintain them- 

 selves. They appear, therefore, to be normally recovered. However, these 

 animals still show impaired motivation for food and water. Adding a 

 sHght amount of quinine to their water, as little as 0.005 per cent is sufficient 

 to cause them to refuse it completely day after day, become dehydrated, 

 stop eating, and die. Normal animals, as mentioned earlier, will take 200 

 times as much quinine, up to 1 per cent, which is poisonous. In the same 

 way, adding a sHght amount of quinine to their food will cause lateral 

 hypothalamic recovered animals to reject it entirely and to starve. Normal 

 animals overcome the barrier to ingestion imposed by a strong negative 

 taste and continue to eat and regulate normally. 



Misleading interpretations of the lateral hypothalamic syndrome have 

 resulted when investigators have offered these rats ordinary food and 

 assumed that because they do not eat that they cannot eat. In these situa- 

 tions, death is an artifact — an artifact of the narrow range of acceptability 

 demonstrated by lateral hypothalamic animals. Normal animals accept a 

 wide range of foods from aversive to highly palatable substances. Lateral 

 hypothalamic animals do not. Early in recovery they will completely 

 refuse even ordinary foods such as purine powder or pellets and will die. 

 But had they been offered more palatable foods, such as liquid diet, milk 

 chocolate or wet cookies, they would have eaten, and, if more advanced in 

 recovery, even regulated their intake perfectly. When sufficient motivation 

 has been regained, taste and smell become less essential for intake. The 

 animal will feed itself intragastrically without taste or smell, but by making 

 the food or water a little less palatable, it can be thrown back into what 

 appears to be the initial stages of aphagia and adipsia. Therefore, they still 

 do not have the full vigorous urge to eat, and in fact, they may never com- 

 pletely recover it. 



On the basis of these results with animals with hypothalamic damage, we 

 may assign to taste and smell their rightful roles in the quantitative regula- 

 tion of food intake. Normal regulation depends on adequate motivation. 

 Taste and smell are powerful motivating stimuli. They are psychic ener- 

 gizers that contribute to the animal's hunger drive. However, in the normal 

 animal, retaining intact all other sources of the urge to eat, they are dis- 

 pensable. But when the drive is diminished by central neural damage, the 

 importance of taste and smell is magnified, and they may become the 

 dominant motives to eat. Therefore, whenever motivation is impaired, 

 taste and smell are essential for regulation. 



