One intraperitoneal injection of goldthioglucose may produce in mice very specific brain lesions followed by a period of hyperphagia leading to obesity. The question is raised whether or not the brain lesions affect feeding behaviour only or that besides this changes in non-feeding behaviour may also contribute to the hyperphagia and obesity observed. Feeding of solitary mice was recorded automatically during 24 h periods after o, 12 and 24 hours of food deprivation and after the GTG treatment. It was found that after GTG injection the mice temporarily (dynamic hyperphagic phase) behave very much like intact hungry ones in that they 1) eat large amounts of food a day 2) gnaw off a bit of food rapidly 3) show little non-feeding behaviour during a meal 4) ingest much food per meal. This period is followed by a static phase during which food intake is somewhat above normal, while the animals show again about normal feeding patterns. Direct observation of the behaviour of solitary mice showed the following: 1) The tendency to sleep has increased permanently and is not related to the occurring obesity. 2) The tendency to climb and to explore the cage has decreased permanently. 3) During a meal non-feeding behaviour occurs rarely. 4) The tendency to groom is not affected. 5) Some (perhaps all) behaviours are less stabile now, as is indicated by the increased occurrence of interruptions. Social behaviour of GTG treated males has been changed drastically as was established by direct observation. It was found that these males, whether or not obese, only rarely fight with other males and that they have a very low tendency to mate. They show a high tendency to flee but on the other hand they often approach the partner although in a very cautious way. However, it was also found that hungry GTG treated mice may fight for their food. This complex change in behaviour patterns of GTG treated mice is discussed briefly and it is concluded that, a. probably the behaviour changes observed are the result of a number of independent effects of the brain lesions, b. the hyperphagia and resulting obesity can be explained largely by a specific lesion in satiety areas of the brain, c. the phenomenon of finickiness, as described by other authors, in the obese animals may be the result of changes in non-feeding behaviour, d. the extreme hunger drive of the dynamic hyperphagic animals may mask signs of finickiness and even enable them to fight for their food, although their aggressiveness in other respects has decreased markedly.