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

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 dorso­ medial 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 syn­ drome ," 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 feed­ ing 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 "sensori­ motor syndrome" period, the other three tests extended well beyond the period where temporary deficits provide a viable explanation of fmdings. METHOD SUbjects Six 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 plastic cages in a temperature<ontrolled laboratory under a regular 12-h­ light/12-h-<lark schedule and had access to Purina Lab Chow and water in the home cage. While all animals were, on other occa­ sions during the 65-<lay postsurgery period, also serving as drug<ontrol subjects in a lesion-<lrug study, no subject received any drug injection during the entire period of assessment.