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Unformatted text preview: logical relatives
of persons with generalized anxiety disorder are more likely than nonrelatives to have
the disorder also (Wetherell et al., 2006; Hettema et al., 2005, 2003). Approximately
15 percent of the relatives of people with the disorder display it themselves—much
more than the prevalence rate found in the general population. And the closer the relative (an identical twin, for example), the greater the likelihood that he or she will also
have the disorder (APA, 2000). Biological Explanations: GABA Inactivity In recent decades important discoveries by brain researchers have offered clearer evidence that generalized anxiety
disorder is related to biological factors. One of the first such discoveries occurred in the
1950s, when researchers determined that benzodiazepines, the family of drugs that
includes alprazolam (Xanax), lorazepam (Ativan), and diazepam (Valium), provide relief
from anxiety. At first, no one understood why benzodiazepines reduce anxiety. Eventually, however, the development of radioactive techniques enabled researchers to pinpoint
the exact sites in the brain that are affected by benzodiazepines (Mohler & Okada, 1977).
Apparently certain neurons have receptors that receive the benzodiazepines, just as a lock
receives a key.
Investigators soon discovered that these benzodiazepine receptors ordinarily receive
gamma-aminobutyric acid (GABA), a common neurotransmitter in the brain. As
you read in Chapter 2, neurotransmitters are chemicals that carry messages from one
neuron to another. GABA carries inhibitory messages: When GABA is received at a receptor, it causes the neuron to stop firing.
On the basis of such findings, biological researchers eventually pieced together
several scenarios of how fear reactions may occur. A leading one began with the notion that in normal fear reactions, key neurons throughout the brain fire more rapidly,
triggering the firing of still more neurons and creating a general state of excitability
throughout the brain and body. Perspiration, breathing, and muscle tension increase.This
state is experienced as fear or anxiety. Continuous firing of neurons eventually triggers
a feedback system—that is, brain and body activities that reduce the level of excitability.
Some neurons throughout the brain release the neurotransmitter GABA, which then
binds to GABA receptors on certain neurons and instructs those neurons to stop firing.
The state of excitability ceases, and the experience of fear or anxiety subsides (Ator,
2005; Costa, 1985, 1983).
Some researchers have concluded that a malfunction in this feedback system can
cause fear or anxiety to go unchecked (Roy-Byrne, 2005). In fact, when investigators
reduced GABA’s ability to bind to GABA receptors, they found that animal subjects
reacted with a rise in anxiety (Costa, 1985; Mohler et al., 1981). This finding
suggested that people with generalized anxiety disorder might have ongoing problems in their anxiety feedback system. Perhaps they have too few
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