The effects of selective ibotenate lesions of the complete hippocampus (CHip), the hippocampal ventral pole (VP), or the medial prefrontal cortex (mPFC) in male rats were assessed on several measures related to energy regulation (i.e., body weight gain, food intake, body adiposity, metabolic activity general behavioral activity, conditioned appetitive responding). The testing conditions were designed to minimize the nonspecific debilitating effects of these surgeries on intake and body weight. Rats with CHip and VP lesions exhibited significantly greater weight gain and food intake compared to controls. Furthermore, CHip-lesioned rats, but not rats with VP lesions, showed elevated metabolic activity, general activity in the dark phase of the light-dark cycle, and greater conditioned appetitive behavior, compared to control rats without these brain lesions. In contrast, rats with mPFC lesions were not different from controls on any of these measures. These results indicate that hippocampal damage interferes with energy and body weight regulation, perhaps by disrupting higher-order learning and memory processes that contribute to the control of appetitive and consummatory behavior.Much research on the causes of overeating and excessive weight gain has been directed at identifying the brain regions where metabolic and hormonal signals that stimulate or suppress intake are detected and utilized (Benoit et al., 2004;Cummings and Overduin, 2007;Leibowitz and Wortley, 2004;Seeley et al., 2004). Although specification of these physiological substrates will be central to any comprehensive account of food intake regulation, it is now clear that such accounts must also consider the role of learning and memory in the control of eating and appetitive behavior (Davidson et al., 2005;Higgs, 2005;Sclafani, 1997;Woods and Ramsay, 2000). In recent years, the hippocampus, a brain structure long considered critical to the performance of a number of learning and memory functions (Eichenbaum, 2006;Squire, 2004), has received increasing attention related to its potential involvement in energy regulation.This increased interest in possible involvement of hippocampus in energy regulation is based, in part, on findings that neurohormonal signals involved with meal termination (e.g., cholecystokinin), meal initiation, (e.g., ghrelin) and signaling the status of bodily energy Please correspond with: Terry L. Davidson,

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The present research investigated the hypothesis that the hippocampus is involved with the control of appetitive behavior by interoceptive “hunger’ and “satiety” signals. Rats were trained to solve a food deprivation intensity discrimination problem in which stimuli produced by 0-h and 24-h food deprivation served as discriminative cues for the delivery of sucrose pellets. For Group 0+, sucrose pellets were delivered at the conclusion of each 4-min session that took place under 0-h food deprivation, whereas no pellets were delivered during sessions that took place when the rats had been food deprived for 24-h. Group 24+ received the reverse discriminative contingency (i.e., they received sucrose pellets under 24-h but not under 0-hr food deprivation). When asymptotic discrimination performance was achieved (indexed by greater incidence of food magazine approach behavior on reinforced compared to nonreinforced sessions), half the rats in each group received hippocampal lesions and the remaining rats in each group were designated as sham- or nonlesioned controls. Following recovery from surgery, food deprivation discrimination performance was compared for lesioned and control rats in both Groups 0+ and 24+. Discriminative responding was impaired for rats with hippocampal lesions relative to their controls. This impairment was based largely on elevated responding to nonreinforced food deprivation cues. In addition, hippocampal damage was associated with increased body weight under conditions of ad libitum feeding. The results suggest that the inhibition of appetitive behavior by energy state signals may depend, in part, on the hippocampus.

Previously, Solomon (1977) reported that aspiration lesions of the dorsal hippocampus in rabbits had no effect either on the acquisition of Pavlovian conditioned inhibition or on performance during a subsequent retardation test. The present experiment confirmed and extended these findings by showing that rats with ibotenate lesions of the complete hippocampus (the dorsal and ventral hippocampus and the dentate gyrus) were also unimpaired on the same types of tasks. Additional tests with the same rats showed that removing the hippocampus significantly impaired extinction of responding to a stimulus that had been previously trained with an appetitive unconditioned stimulus. The performance of the lesioned rats on a summation test was also marginally, but not significantly, different from that of controls. The data are discussed with reference to the idea that the hippocampus is involved with the formation of some, but not all, types of inhibitory associations.

It is generally assumed that fluoxetine does not produce cognitive impairments, based on observations that fluoxetine-treated animals do not show impairment in learning the spatial water-maze task. As fluoxetine has different effects on different brain regions and as learning is not a unitary phenomenon, it may be the case that fluoxetine has different effects on different types of learning and memory paradigms. In this study, 15 male Sprague-Dawley rats were given chronic injections of either fluoxetine or saline and received training in two hippocampal-independent tasks in addition to a spatial water-maze task. The two hippocampal-independent tasks were a short-delay appetitive Pavlovian-conditioning task and an object-recognition task. The results showed that the fluoxetine-injected rats did not show any impairment relative to the saline controls in either the acquisition or the retention phases of the water-maze task, but were significantly impaired in both of the hippocampal-independent tasks. Fluoxetine-injected rats spent significantly less time exploring the novel object in the object-recognition task and took longer to learn the association between the conditional stimulus and the appetitive unconditional stimulus in the appetitive Pavlovian-conditioning task.