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By John B. Arden, Lloyd Linford

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Additional info for Brain-Based Therapy with Adults: Evidence-Based Treatment for Everyday Practice

Sample text

Similarly, the prefrontal cortex appears capable of modulating the release of stress hormones (Diorio, Viace, & Meany, 1993), but when the amygdala ignores or overrides it, this inhibitory function of the cortex is less efficient, in effect taking the brakes off the amygdala and setting off a reaction pattern that leads to escalating stress hormones and ‘‘new learning’’ that is more resistant to extinction (LeDoux, 1996). The hippocampus (from the classical Greek name for ‘‘seahorse’’ because it is so shaped) is a complexly organized limbic structure.

There appears to be a reciprocal relationship between the amygdala and cortex. McGaugh (2004), for example, has developed the memory modulation hypothesis, which asserts that following an arousing emotional experience, corticosteroid and adrenergic systems are activated by the amygdala, leading to enhanced consolidation of memory by the cortex. Similarly, the prefrontal cortex appears capable of modulating the release of stress hormones (Diorio, Viace, & Meany, 1993), but when the amygdala ignores or overrides it, this inhibitory function of the cortex is less efficient, in effect taking the brakes off the amygdala and setting off a reaction pattern that leads to escalating stress hormones and ‘‘new learning’’ that is more resistant to extinction (LeDoux, 1996).

The brain, in other words, is duped into being plastic by these treatments’’ (emphasis added). Many serotonin fibers terminate in a part of the brain called the amygdala, which encodes incoming perceptual data with emotional coloring. Serotonin actually excites the GABA cells—and GABA has an inhibitory effect—increasing the inhibiting influence of these cells on projection neurons. Medications such as fluoxetine (Prozac) may work in the amygdala to reduce the activity of the projection neurons and consequently modulate anxiety.

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