Three brain areas of panic disorder patients are lacking in a key component of a chemical messenger system that regulates emotion, researchers at the NIHs National Institute of Mental Health (NIMH) have discovered. Brain scans revealed that a type of serotonin receptor is reduced by nearly a third in three structures straddling the center of the brain. The finding is the first in living humans to show that the receptor, which is pivotal to the action of widely prescribed anti-anxiety medications, may be abnormal in the disorder, and may help to explain how genes might influence vulnerability. Drs. Alexander Neumeister and Wayne Drevets, NIMH Mood and Anxiety Disorders Program, and colleagues, report on their findings in the January 21, 2004 Journal of Neuroscience.
Each year, panic attacks strike about 2.4 million American adults "out of the blue," with feelings of intense fear and physical symptoms sometimes confused with a heart attack. Unchecked, the disorder often sets in motion a debilitating psychological sequel syndrome of agoraphobia, avoiding public places. Panic disorder runs in families and researchers have long suspected that it has a genetic component. The new finding, combined with evidence from recent animal studies, suggests that genes might increase risk for the disorder by coding for decreased expression of the receptors, say the researchers.
NIMH grantee Dr. Rene Hen, Columbia University, and colleagues, reported in 2002 that a strain of gene "knockout" mice, engineered to lack the receptor during a critical period in early development, exhibit anxiety traits in adulthood, such as a reluctance to begin eating in an unfamiliar environment. More recent experiments with the knockout mice show that a popular SSRI (serotonin selective reuptake inhibitor) drug produces its anti-anxiety effects by stimulating the formation of new neurons in the hippocampus via the serotonin 5-HT1A receptor.
Jules Asher | EurekAlert!
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