such as "Introduction", "Conclusion"..etc
It has been known for over a century that the temporal lobe,including the amygdala, is involved in emotion. In 1888, Brownand Schafer (21) described taming in monkeys affect associatedwith temporal lobe retraction. Klüver and Bucy (102) elaboratedon this finding by characterizing a collection of emotionaldisturbances caused by temporal lobe damage, which became knownas Klüver-Bucy syndrome. Monkeys with temporal lobe lesionsexhibited an absence of anger and fear, increased exploration,visual agnosia, hyperorality, hypersexualtity, and loss of socialinteractions. Subsequent work has shown that lesions restrictedto the amygdala produced many of these effects including aloss of fear and anger, increased exploration, and hyperorality(288, 300). The reduced fear and anger, "taming" effect,of amygdalar lesions is seen in many animal species (71). Whileamygdala damage in humans rarely results in full-blown Klüver-Bucysyndrome, it is associated with some emotional deficits (2)including loss of the recognition of fear in others (1).
Our understanding of the amygdala and its role in emotion ishampered by the abstract nature of emotion itself. In humans,bilateral damage restricted to the amygdala is extremely rare.Animal studies are limited by their inability to tell us howthey "feel." Thus much of our understanding of the role ofthe amygdala in emotion comes from the animal studies on fear(115). Fear, conditioned and unconditioned, elicits a constellationof autonomic and hormonal responses that include cardiac effects(increased blood pressure, changes in heart rate), hormonaleffects (release of stress hormones, adrenaline), defecation,vocalization, freezing, and a potentiated startle response(20, 115, 116, 141). These fear response patterns are similarin animals and humans (110). Electrical stimulation of theamygdala elicits fear and anxiety responses in both humans (34, 70) and animals (94), and lesions of the amygdala blockthe expression of certain, but not all, types of unconditionedfear. For example, rats with amygdala lesions show reducedfreezing in response to cats (17) or cat hair (276), attenuatedanalgesia and heart rate responses to a loud noise (14, 298),and have reduced taste neophobia (182). However, amygdalalesions do not affect other measures of fear such as open armavoidance in an elevated plus maze (271, 272) or analgesiato shock (287).
The amygdala is also necessary for many types of fear-motivatedlearning. Amygdala lesions disrupt the acquisition, but notthe retention, of both active avoidance (escape from fear)(212) and passive avoidance (124, 235, 271) conditionedresponses. Moreover, emotional processing in the amygdala isnot limited to fear and aversive stimuli. The amygdala is alsoinvolved in conditioning using appetitive stimuli such as food,sex, and drugs. Amygdalar lesions disrupt appetitive Pavlovianconditioning (66, 266), conditioned place preference (54,55, 166), and conditioned taste aversion (180, 182, 230,292) and reduce gustatory neophobia (51, 266). Finally, inaddition to the direct role of the amygdala in learning andmemory, activation of the amygdala also has a modulatory effecton the acquisition and consolidation of memories that evokean emotional response (168, 169, 195). Although it is wellrecognized that the amygdala is involved in a myriad of memory-and learning-related tasks, the best studied is its role inPavlovian fear conditioning and fear-motivated operant conditioning.The remainder of this review will therefore focus on the neuralsubstrates of classical fear conditioning.
Enter the code exactly as it appears. All letters are case insensitive, there is no zero.