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Adult female ocelots (Felis pardalis) were treated with one of four dosages of equine chorionic gonadotrophin (eCG) and human chorionic gonadotrophin (hCG) (100 iu eCG/75 iu hCG, n = 3; 200 iu eCG/150 iu hCG, n = 4; 400 iu eCG/150 iu hCG, n = 5; 500 iu eCG/225 iu hCG, n = 5); hCG was administered 80 h after eCG. Ovaries of each animal were evaluated by laparoscopy 39-43 h after hCG, and blood was collected for progesterone and oestradiol analysis. With progressive increases in gonadotrophin dosage, female ocelots produced more (P< 0.05) unovulated follicles (> or = 2 mm in diameter), ranging from 1.3 +/- 0.7 (mean +/- SEM) follicles per female at the lowest dosage to 8.8 +/- 2.8 follicles per female at the highest dosage. Similarly, ocelots produced more (P < 0.05) corpora lutea with increasing gonadotrophin dosages, with mean values ranging from 0-5.0 +/- 1.2 corpora lutea. However, across treatment groups, a similar proportion (P > 0.05) of females ovulated in response to each dosage. At laparoscopy, serum concentrations of oestradiol (overall mean, 330.2 +/- 62.2 pg ml-1) and serum concentrations of progesterone (overall mean, 18.5 +/- 6.4 ng ml-1) in ovulating females did not differ (P > 0.05) across treatment groups. Ten ovulating ocelots were laparoscopically inseminated with fresh (4.7 +/- 0.2 x 10(6); n = 2 females) or frozen-thawed (10.7 +/- 1.8 x 10(6); n = 8 females), motile spermatozoa. One female treated with 500 iu eCG/225 iu hCG and inseminated with 7.5 x 10(6) motile, frozen-thawed spermatozoa conceived and gave birth to a healthy male kitten after a gestation of 78 days. We conclude that ocelots are relatively insensitive to exogenous gonadotrophins, requiring much higher dosages (on a per body mass basis) to elicit an appropriate ovarian response than do any other felid species studied to date. Nonetheless, the gonadotrophin-treated female can become pregnant and carry offspring to term after laparoscopic intrauterine insemination with frozen-thawed spermatozoa.

SUMMARYNeuronal activity related to brain-stimulation reward and to feeding was analyzed in rhesus monkeys and squirrel monkeys as follows. First, self-stimulation of the lateral hypothalamus, orbitofrontal cortex, amygdala and nucleus accumbens was found. Second, a population of single neurones in the lateral hypothalamus was found to be trans-synaptically activated from one or several self-stimulation sites. It was also found that populations of neurones in the orbitofrontal cortex and amygdala were activated from at least some of the self-stimulation sites. Thus, in the monkey, there is evidence for an interconnected set of self-stimulation sites, stimulation in any one of which may activate neurones in the other regions. These sites include the lateral hypothalamus, amygdala, and orbitofrontal cortex. Third, in one sample of 764 neurones in the lateral hypothalamus and substantia innominata which were activated from brainstimulation reward sites, 13.6 ~ were also activated during feeding, by the sight and/or taste of food. The responses of the neurones with activity associated with taste occurred only while some substances (e.g. sweet substances such as glucose) were in the mouth, depended on the concentration of the substances being tasted, and were independent of mouth movements made by the monkeys. Fourth, the responses of these neurones occurred to food when the monkeys were hungry, but not when they were satiated. Fifth, self-stimulation occurred in the region of these neurones in the lateral hypothalamus and substantia innominata, and was attenuated by satiety. These results suggest that self-stimulation of some brain sites occurs because of activation of neurones in the lateral hypothalamus and substantia innominata activated by the sight

SUMMARYNeurones in the lateral hypothalamic region are described which alter their firing rates when a monkey looks at food. The units responded when the monkey looked at different types of food, but not at non-food objects or simple visual stimuli. The units did not respond in relation to motor movements, intense arousal, nor when a salient aversive stimulus was shown, nor in relation to eye movements, and were thus shown to be different from units in the globus pallidus which did respond in some of these control tests. The neurones did not respond to olfactory stimuli and did not respond if the animal ate in the dark. Because of these findings it is suggested that the activity of these hypothalamic neurones is associated with the sight of food. It is of interest that these neurones which respond when food is shown to a hungry animal are found in a region thought to be involved in the control of feeding.

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In Experiment 1, intact rats were given either lactose or sucrose solutions. Although on first exposure they readily consumed lactose, its ingestion produced a conditioned taste avoidance which was partly extinguished by repeated sucrose exposure after lactose conditioning. In Experiment 2, rats with large bilateral electrolytic lesions of the basolateral amygdala and those with either sham or no operations were given two pairings of saline with LiCl injections (upper gastrointestinal tract discomfort) and in a separate condition access to high levels of lactose (lower gastrointestinal tract discomfort). Conditioned taste avoidances were measured both by two-bottle tests and by video recordings of the rats' orofacial and somatic responses. The lesions attenuated LiCl-induced taste aversion but not lactose-induced taste avoidance, results demonstrating that taste avoidance can occur without the basolateral amygdala. The results suggested that aversions based on distaste can be distinguished from avoidances based on danger, not only in terms of orofacial responses but also in terms of their neuroanatomical substrate.

I The effects of three doses of fenfluramine on feeding and drinking in the rat were examined. 2 Feeding and drinking were subdivided into meals and bouts, and the changes in feeding/drinking were expressed in terms of meal/bout frequency, meal/bout size, meal/bout length, and eating/drinking rate. 3 The changes in these parameters were examined over different time periods after the injection. 4 Significant changes in the distribution of inter-response intervals within meals were found in time period I with 5 mg/kg and 10 mg/kg doses of fenfluramine. Videotape and computer analysis showed that the changes in inter-response interval histograms differed significantly from those seen in normal animals approaching satiety. Drinking parameters also changed. 5 Compensatory increases in feeding were observed in time period 4 with the 10 mg/kg dose. 6 The difficulties in designing and interpreting experiments in feeding are discussed, and the action of fenfluramine as an anorectic drug is considered.