Abstract:Electrophysiologic and lesion studies of animals increasingly implicate the amygdala in aspects of emotional processing. Yet, the functions of the human amygdala remain poorly understood. To examine the contributions of the amygdala and other limbic and paralimbic regions to emotional processing, we exposed healthy subjects to aversive olfactory stimuli while measuring regional cerebral blood f low (rCBF) with positron emission tomography. Exposure to a highly aversive odorant produced strong rCBF increases in… Show more
“…The link between drug craving and OFC activity is the most common association found in this type of functional imaging work, and has led to the hypothesis that the OFC mediates drive and compulsive behavior associated with drug dependence (Volkow and Fowler, 2000). This region is also thought to mediate decision making that leads to reward (London et al, 2000;O'Doherty et al, 2001a;Ernst et al, 2002) and to act as a secondary processing center for gustatory (Zald et al, 1998;O'Doherty et al, 2001b) and olfactory (Zatorre et al, 1992;Levy et al, 1997;Zald and Pardo, 1997) stimuli. These putative functions of the OFC may help explain the consistent positive association between metabolism in this region and craving.…”
In untreated smokers, exposure to cigarette-related cues increases both the intensity of cigarette craving and relative glucose metabolism of the perigenual/ventral anterior cingulate cortex (ACC). Given that treatment with bupropion HCl reduces overall cigarette craving levels in nicotine dependent subjects, we performed a preliminary study of smokers to determine if bupropion HCl treatment attenuates cue-induced cigarette craving and associated brain metabolic activation. Thirtyseven, otherwise healthy smokers (20 untreated and 17 who had received open-label treatment with bupropion HCl) underwent two 18 F-fluorodeoxyglucose positron emission tomography scanning sessions in randomized order-one when presented with neutral cues and the other when presented with cigarette-related cues. Bupropion-treated smokers had smaller cigarette cue-induced increases in craving scores on the Urge to Smoke (UTS) Scale and less activation of perigenual/ventral ACC metabolism from the neutral to the cigarette cue scan than untreated smokers. Thus, in addition to its known effects on spontaneous cigarette craving and withdrawal symptoms, bupropion HCl diminishes cue-induced cigarette craving and appears to attenuate cigarette cue-induced ACC activation. These results are consistent with the known effects of bupropion HCl, including its enhancement of catecholaminergic neurotransmission.
“…The link between drug craving and OFC activity is the most common association found in this type of functional imaging work, and has led to the hypothesis that the OFC mediates drive and compulsive behavior associated with drug dependence (Volkow and Fowler, 2000). This region is also thought to mediate decision making that leads to reward (London et al, 2000;O'Doherty et al, 2001a;Ernst et al, 2002) and to act as a secondary processing center for gustatory (Zald et al, 1998;O'Doherty et al, 2001b) and olfactory (Zatorre et al, 1992;Levy et al, 1997;Zald and Pardo, 1997) stimuli. These putative functions of the OFC may help explain the consistent positive association between metabolism in this region and craving.…”
In untreated smokers, exposure to cigarette-related cues increases both the intensity of cigarette craving and relative glucose metabolism of the perigenual/ventral anterior cingulate cortex (ACC). Given that treatment with bupropion HCl reduces overall cigarette craving levels in nicotine dependent subjects, we performed a preliminary study of smokers to determine if bupropion HCl treatment attenuates cue-induced cigarette craving and associated brain metabolic activation. Thirtyseven, otherwise healthy smokers (20 untreated and 17 who had received open-label treatment with bupropion HCl) underwent two 18 F-fluorodeoxyglucose positron emission tomography scanning sessions in randomized order-one when presented with neutral cues and the other when presented with cigarette-related cues. Bupropion-treated smokers had smaller cigarette cue-induced increases in craving scores on the Urge to Smoke (UTS) Scale and less activation of perigenual/ventral ACC metabolism from the neutral to the cigarette cue scan than untreated smokers. Thus, in addition to its known effects on spontaneous cigarette craving and withdrawal symptoms, bupropion HCl diminishes cue-induced cigarette craving and appears to attenuate cigarette cue-induced ACC activation. These results are consistent with the known effects of bupropion HCl, including its enhancement of catecholaminergic neurotransmission.
“…Nevertheless, highly significant correlations were observed in the present study between odor threshold and volume of the amygdala in normal elderly persons (see Table 3). Only rarely in neuroimaging studies of olfaction has activation been detected in mesial temporal areas of amygdala (Cerf-Ducastel & Murphy, 2001;Small et al, 1997;Sobel et al, 2000;Zald & Pardo, 1997, entorhinal cortex (Cerf-Ducastel & Murphy, 2001;Levy et al, 1997;Zald & Pardo, 2000), parahippocampal gyrus, or hippocampus (Cerf-Ducastel & Murphy, 2001;Levy et al, 1997;Small et al, 1997;Zald & Pardo, 2000); although electrophysiological and anatomical studies indicate that the anterior cortical nucleus of the amygdala, the periamygdaloid area and the lateral entorhinal cortex receive direct projections from the olfactory bulb through the lateral olfactory track (Biella & De Curtis, 2000;Carmichael et al, 1994;Price, 1985;1987). The entorhinal area also receives olfactory projections from the amygdaloid area and the piriform cortex.…”
The very high sensitivity and specificity of odor identification tasks in discriminating between Alzheimer's patients and normals suggests that they reflect the presence of underlying neuropathology. Significant neuropathological changes are seen in areas critical to processing olfactory information, even in the early stages of Alzheimer's disease (AD). The current study was designed to investigate whether performance on olfactory tasks (odor threshold and odor identification) was related to volumetric MRI measures of mesial temporal areas central to olfactory information processing and important in the neuropathology of AD. Participants were 8 male and 5 female patients with probable AD, and 10 male and 12 female normal age-matched controls, diagnosed at the UCSD Alzheimer's Disease Research Center. The study investigated correlations between volumetric measures of hippocampus, the parahippocampal gyrus and the amygdala, and the psychophysical measures of olfactory function. Robust relationships were observed between mesial temporal lobe volumes and olfactory functional measures. The finding of a strong relationship between left hippocampal volume and performance on the odor identification task (r 5 .85) is compatible with a left-hemisphere superiority for verbally mediated olfactory tasks. The findings suggest a neural substrate for the breakdown in functional performance on verbally mediated odor identification tasks in Alzheimer's disease and suggest the utility of quantitative MRI measures and psychophysical performance in the assessment of AD. These results support the potential clinical utility of inclusion of odor identification tests in diagnostic batteries for detecting AD. (JINS, 2003, 9, 459-471.)
“…In humans, in addition to activation of the pyriform (olfactory) cortex, [56][57][58] there is strong and consistent activation of the OFC by olfactory stimuli, 49,59 and this region seems to represent the pleasantness of odour, as shown by a sensory-specific satiety experiment with banana vs vanilla odour. 60 Further, pleasant odours tend to activate the medial, and unpleasant odours the more lateral, OFC, 61 adding to the evidence that it is a principle that there is a hedonic map in the OFC, and also in the ACC, which receives inputs from the OFC.…”
Complementary neuronal recordings and functional neuroimaging in humans, show that the primary taste cortex in the anterior insula provides separate and combined representations of the taste, temperature and texture (including fat texture) of food in the mouth independently of hunger and thus of reward value and pleasantness. One synapse on, in the orbitofrontal cortex (OFC), these sensory inputs are for some neurons combined by learning with olfactory and visual inputs, and these neurons encode food reward in that they only respond to food when hungry, and in that activations correlate with subjective pleasantness. Cognitive factors, including word-level descriptions, and attention, modulate the representation of the reward value of food in the OFC. Further, there are individual differences in the representation of the reward value of food in the OFC. It is argued that overeating and obesity are related in many cases to an increased reward value of the sensory inputs produced by foods, and their modulation by cognition and attention, which overrides existing satiety signals. It is proposed that control of all rather than one or several of these factors that influence food reward and eating may be important in the prevention and treatment of overeating and obesity.
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