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. 2004 Jun 16;24(24):5506-15.
doi: 10.1523/JNEUROSCI.0292-04.2004.

The role of the central nucleus of the amygdala in mediating fear and anxiety in the primate

Ned H Kalin  1 , Steven E Shelton, Richard J Davidson
Affiliations

The role of the central nucleus of the amygdala in mediating fear and anxiety in the primate

Ned H Kalin et al. J Neurosci. .

Abstract

Numerous studies demonstrate that the rhesus monkey is an excellent species with which to investigate mechanisms underlying human emotion and psychopathology. To examine the role of the central nucleus of the amygdala (CeA) in mediating the behavioral and physiological responses associated with fear and anxiety, we used rhesus monkeys to assess the effects of excitotoxic lesions of the CeA. Behavioral and physiological responses of nine monkeys with bilateral CeA destruction (ranging from 46 to 98%) were compared with five animals with asymmetric lesions (42-86.5% destruction on the most affected side) and with 16 unoperated controls. Results suggest that similar to rodent species, the primate CeA plays a role in mediating fear- and anxiety-related behavioral and endocrine responses. Compared with controls and the asymmetric-lesion group, bilaterally lesioned monkeys displayed significantly less fear-related behavior when exposed to a snake and less freezing behavior when confronted by a human intruder. In addition, bilaterally lesioned monkeys had decreased levels of CSF corticotrophin-releasing factor (CRF), and both lesioned groups had decreased plasma ACTH concentrations. In contrast to these findings, patterns of asymmetric frontal brain electrical activity, as assessed by regional scalp EEG, did not significantly differ between control and lesioned monkeys. These findings suggest that in primates, the CeA is involved in mediating fear- and anxiety-related behavioral and pituitary-adrenal responses as well as in modulating brain CRF activity.

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Figures

Figure 1.
Figure 1.
a, Coronal sections through the amygdala demonstrating the boundaries of the CeA. The CeA is located in the dorsal amygdala and is outlined to the left. b, Coronal sections from an intact and an ibotenic acid-lesioned animal demonstrate the boundaries of the CeA and the extent of a lesion. The top row displays coronal sections from the left hemisphere through the middle of the amygdala. The hemisected brain at the far left shows the region, in blue, from which the magnified coronal sections were taken. The CeA is depicted in yellow. The first two magnified coronal sections are Nissl stained, and the last two sections are stained with GFAP. The CeA is outlined in the intact sections, whereas in the lesioned sections, arrows indicate the boundaries of the lesion. The middle row displays comparable sections through the posterior amygdala. The bottom row of the figure shows the neuronal loss and glial infiltration in the lesioned compared with the intact CeA (400× magnification). At the far left, the CeA is depicted in yellow, and the area from which the magnified sections were selected is displayed in red.
Figure 2.
Figure 2.
Four coronal sections through the anterior to posterior extent of the CeA are displayed showing the amount of CeA damage in bilateral-lesion (a) and a symmetric-lesion (b) groups. The intact CeA is depicted in blue, the area of the total lesion is displayed in yellow, and the CeA region that is lesioned is depicted in green. These sections are a subset of the 14 coronal slices that contain the CeA and that were used to define the percentage of CeA damage. The percentage destruction of CeA in each hemisphere and the total amount of CeA destruction are noted for each animal.
Figure 2.
Figure 2.
Four coronal sections through the anterior to posterior extent of the CeA are displayed showing the amount of CeA damage in bilateral-lesion (a) and a symmetric-lesion (b) groups. The intact CeA is depicted in blue, the area of the total lesion is displayed in yellow, and the CeA region that is lesioned is depicted in green. These sections are a subset of the 14 coronal slices that contain the CeA and that were used to define the percentage of CeA damage. The percentage destruction of CeA in each hemisphere and the total amount of CeA destruction are noted for each animal.
Figure 2.
Figure 2.
Four coronal sections through the anterior to posterior extent of the CeA are displayed showing the amount of CeA damage in bilateral-lesion (a) and a symmetric-lesion (b) groups. The intact CeA is depicted in blue, the area of the total lesion is displayed in yellow, and the CeA region that is lesioned is depicted in green. These sections are a subset of the 14 coronal slices that contain the CeA and that were used to define the percentage of CeA damage. The percentage destruction of CeA in each hemisphere and the total amount of CeA destruction are noted for each animal.
Figure 3.
Figure 3.
Effects of CeA lesions on freezing duration in the human intruder paradigm. For analysis, the data were transformed to achieve normality (F = 4.330; df 2, 27; p < 0.023). Duncan post hoc test: **p < 0.01 differs from all groups.
Figure 4.
Figure 4.
Effects of CeA lesions on snake fear as determined by the monkeys' latency to reach for a treat in the presence of snake stimuli compared with a neutral stimulus and no stimulus. The object by lesion interaction was significant (F = 2.88; df 6, 78; p < 0.014). Duncan post hoc test: **p < 0.01 differs from bilateral group.
Figure 5.
Figure 5.
Effects of CeA lesions on plasma ACTH concentrations (a)(F = 3.629; df 2, 27; p < 0.04) and CSF CRF concentrations (b) (F = 3.30; df 2, 27; p = 0.052). Duncan post hoc test: *p < 0.05, bilateral group differs from control group; **p < 0.01, control differs from other groups.
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