Hunger and satiety modify the responses of olfactory and visual neurons in the primate orbitofrontal cortex

Abstract

SUMMARYAND CONCLUSIONS1. The primate orbitofiontal cortex is the site of convergence of information from primary taste and primary olfactory cortical regions. In addition, it receives projections from temporal lobe visual areas concerned with the representation of objects such as foods. Previous work has shown that the responses of gustatory neurons in the secondary taste area within the orbitofrontal cortex are modulated by hunger and satiety, in that they stop responding to the taste of a food on which an animal has been fed to behavioral satiation, yet may continue to respond to the taste of other foods.2. This study demonstrates a similar modulation of the responses of olfactory and visual orbitofrontal cortex neurons after &ding to satiety. Seven of nine olfactory neurons that were responsive to the odors of foods, such as blackcurrant juice, were found to decrease their responses to the odor of the satiating food in a selective and statistically significant manner.3. It also was found for eight of nine neurons that had selective responses to the sight of food, that they demonstrated a sensoryspecific reduction in their visual responses to foods after satiation.4 The responses of orbitofiontal cortex neurons selective for foods in more than one modality also were analyzed before and after feeding to satiation. Satiety often affected the responses of these multimodal neurons across all modalities, but a sensoryspecific effect was not always demonstrable for both modalities.5. These findings show that the olfactory and visual representations of food, as well as the taste representation of food, in the primate orbitofi=ontal cortex are modulated by hunger. Usually a component related to sensory-specific satiety can be demonstrated. The findings link at least part of the processing of olfactory and visual information in this brain region to the control of feedingrelated behavior.

Dopaminergic and non-dopaminergic value systems in conditioning and outcome-specific revaluation

“…The model's response to devaluation, in the CS-FSS (foodspecific satiety) and US-FSS tasks, replicates reported behavioral patterns and electrophysiological neural responses (Rolls et al, 1986;Scott et al, 1995;Critchley and Rolls, 1996;Rolls et al, 1999). Experiments that assay behavioral responses to increasing satiety reveal that animals quickly switch from acceptance to rejection of food rewards such as juice.…”

“…Experiments that assay behavioral responses to increasing satiety reveal that animals quickly switch from acceptance to rejection of food rewards such as juice. In particular, experiments that assay neuronal responses during trials where juice is consumed with increasing satiety have found that neurons have a logistically decreasing response to US or CS presentation as satiety increases (Rolls et al, 1986;Critchley and Rolls, 1996). The model exhibits the FSS property in that both simulated and electrophysiologically recorded neurons in the AMYG, LH, ORB have diminished responses to a sated food, but preserved responses to an unsated food (Rolls et al, 1986;Nishijo et al, 1988a).…”

“…Both the shape of the learning and reversal curves reported by Jagadeesh et al (2001) and the number of trials required for behavioral reversal suggest that a learning based mechanism plays a dominant role in reversal learning, at least for the first few reversals. The slow learning of new contingencies many figures from Critchley and Rolls (1996). 4.4 Predictions and Discussion.…”

The anterior medial temporal lobes: Their role in food intake and body weight regulation

“…Sensory-specific satiety can be defined as the implicit memory for consumed food items, characterized by a decrease in pleasure derived from recently consumed food items while other unconsumed food items are still pleasurable. Sensory-specific satiety is mediated by the orbitofrontal cortex [25] and not by the hippocampus.…”

Neural representations of hunger and satiety in Prader–Willi syndrome

“…However, an imaging study in a control group of nonobese individuals, 12 together with research from other groups, [13][14][15] has shown that the motivation to eat is controlled by an extensive system of reciprocally connected neural areas, beyond the hypothalamus, mediating both the intrinsically derived hunger drive to eat and the extrinsically derived incentive to eat. 12,16 Key brain regions for the former include the hypothalamus 11,[17][18][19] striatum, 20 orbitofrontal cortex (OFC) [21][22][23] insula [24][25][26] and anterior cingulate cortex, 24 and, for the latter, the amygdala and OFC. [27][28][29][30] Indeed, Lucignani et al 31 have found altered cerebral GABA A receptor function in the insula and cingulate, frontal and temporal neocortices in six adults with PWS compared to controls.…”