To investigate the function of the amygdala following traumatic brain
injury (TBI), rats were tested on a gustatory neophobia task that is s
ensitive to amygdala and hippocampaI damage. Rats were either injured
at a moderate level of fluid percussion injury (2.1 atm) or surgically
prepared but not injured (sham-injury). Seven days after injury (n =
8) or sham injury (n = 9), rats were habituated to the testing chamber
without food items present for 30 min. All rats were then food depriv
ed. Twenty-four hours later, rats were placed in the testing chamber f
or 30 min and allowed to eat freely from four dishes of different food
s: rat chow, raisins, potatoes, and cookies. Results showed that injur
ed and sham-injured rats did not differ in their ability to find hidde
n food, suggesting that TBI does not produce an enduring impairment of
olfaction. There was also no difference in the total amount of food e
aten between injured and sham groups (p > 0.05). The percentage of eac
h type of food consumed did differ between the two groups with sham co
ntrols consuming more familiar food (rat chow) compared to the unfamil
iar foods (p < 0.01). The injured animals distributed their eating eve
nly among the four foods with no particular preference for any one foo
d (p > 0.05). This pattern of eating behavior in injured animals is si
milar to animals that have lesions to both the hippocampus and amygdal
a (Sutherland and McDonald, 1990). Therefore, the results of this expe
riment suggest that, in addition to the hippocampus, the amygdala may
also contribute to the behavioral changes observed following TBI.