Dorsomedial amygdala damage: A time-after-surgery assessment of feeding

Abstract

The food consumption of Charles River male rats with dorsomedial amygdala lesions was compared with sham operates and normal controls on four tests spanning a 65-day postsurgery period. Following 24-h food deprivation (18-and 65-day postsurgery tests), lesioned animals ate significantly less than the other two groups (p < .01). Although 24-h food and water deprivation (35-and 50-day postsurgery tests) increased the absolute level of food consumption in all groups, the relative magnitude of the feeding deficit in lesioned animals remained approximately the same (p < .01). The results suggest that hypotheses which stress the "temporary deficit" nature of lesion effects do not adequately explain the changes in feeding following dorsomedial amygdala damage.Changes in feeding behavior after amygdala damage are well documented, with destruction of dorsomedial regions decreasing food consumption (Cole, 1974; F onberg, 1966) and destruction of more basolateral sites increasing food consumption (Fonberg, 1968). While the reduction in feeding by rats following dorsomedial amygdala damage appears to be food·deprivation dependent (Cole, 1974), the similar attenuation of the anorexigenic properties of amphetamine following recovery from dorsomedial amygdala lesions (Cole, 1973) and from lateral hypothalamic lesions (Carlisle, 1964) suggests that adrenergic processes underlie the regulation of feeding in both areas.Evidence suggesting that amygdala damage also alters the subject's sensitivity or responsiveness to environmental stimuli (Nauta, 1963;Sclafani, Belluzzi, & Grossman, 1970;White, 1971) raises the question as to whether these changes in feeding are due to a temporary deficit in responding to stimulus properties of food or represent more stable changes in feeding. Also, Turner (1973) has indicated that medial amygdala lesions produce a rather extensive "sensorimotor syndrome ," characterized by visual and olfactory unre· sponsiveness, absent or sluggish visual and proprioceptive placing, forelimb disuse, and inability to make localized and conditioned responses to somatosensory stimuli. Since recovery from the "sensorimotor syndrome" appears to take place within 10 to 22 days (Turner, 1973), any general effects of such a deficit on feeding behavior should be only temporary.As a means of determining whether changes in feeding following dorsomedial amygdala damage are temporary (and therefore possibly due to transitory deficits) or more stable, the present study reports a preliminary assessment of lesion effects extending over a 65-day postsurgery period. While the first test was conducted toward the end of the proposed "sensorimotor syndrome" period, the other three tests extended well beyond the period where temporary deficits provide a viable explanation of fmdings. METHOD SUbjectsSix amygdala lesion, six sham-operate, and six normal control male Charles River rats were subjects. At the time of surgery, the animals were 120-130 days of age, with body weights ranging from 350450 g. They were housed individually in...

Food-motivated behavior in rats with cortico-basomedial amygdala damage.

“…The lack of increase of body weight in the CBM group between the preoperative and the first postoperative records might be attributed to some loss just after surgery and subsequent compensation up to the 15th postoperative day. This assumption is compatible with the data obtained by Cole (1977), indicating the drop of average body weight by the second day after dorsomedial amygdaloid lesions and the recovery of some of this loss by the 8th postoperative day. Further records in his study, starting from the 18th day, did not disclose any difference in body weight of operated rats with relation to control rats.…”

“…Experiment 2: Food Intake After Short Deprivation Cole (1974Cole ( , 1977 reported that dorsomedial amygdaloid lesions lowered only the 24-hr-deprivation-induced and not spontaneous food intake. On the other hand, in the study of Shoenfeld and Hamilton (1981) none of several groups of rats with various locations of lesions in the amygdala showed a food-deprivation-dependent decrease of feeding.…”

Amygdala-lesion obesity: what is the role of the various amygdaloid nuclei?

“…However, besides aphagia, their rats displayed sensory-motor deficits, including excessive gnawing and spillage of their food pellets. Others have reported similar results for rats, cats, and dogs (e.g., 4,11,19,21). Aphagia is a well-established consequence of damage to the caudal globus pallidus (16,44,48,52,60).…”

“…Studies employing lesions of the corticomedial nuclei were equally mixed, reporting weight gains (26), weight losses (12,58), or no changes in body weight (59,60,63). Central nucleus lesions have similarly been reported to result in either weight/fat gain (7,42), aphagia and/or weight loss (8,11,23), or no change in food intake and body weight (16,29,57,59,60). In recent years, King and colleagues (30)(31)(32)(33)(35)(36)(37)(38)(39)(40) have reported hyperphagia and moderate obesity in female rats given bilateral lesions of the most posterodorsal aspects of the amygdala, with weight gains of 50-80 g typical in the first 15 to 20 days after lesions.…”

Amygdaloid lesion-induced obesity: relation to sexual behavior, olfaction, and the ventromedial hypothalamus

“…Lesions of the corticomedial nuclei similarly were reported to result in weight gain (33,66), weight loss (26,187,216), or no change in body weight (83,120,121,123,145,188,195,201). Studies of the effects of lesions of the central nucleus were equally conflicting, reporting weight or fat gain (14,138), weight loss (15,25,56,216), or no change (24,34,84,180,195).…”