Panic Disorder Patients Found Deficient in Emotion Regulating Receptor; May Lead to Better Treatments
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PANIC DISORDER PATIENTS FOUND DEFICIENT IN EMOTION REGULATING RECEPTOR; MAY LEAD TO BETTER TREATMENTS
WASHINGTON, DC January 23, 2004 – A new finding, combined with evidence from recent animal studies, suggests that genes might increase risk for panic disorder by coding for decreased expression of specific receptor molecules.
The finding is the first in humans to show that a receptor, which is pivotal to the action of widely prescribed anti-anxiety medications, may be abnormal in the disorder and help to explain how genes might influence vulnerability.
In the study, positron emission tomography (PET) determined that three brain areas of panic disorder patients are lacking in a key component of a chemical messenger system that regulates emotion, says Alexander Neumeister, MD, of the National Institute of Mental Health (NIMH). Brain scans revealed that the component, a type of serotonin receptor, is reduced by nearly a third in three structures straddling the center of the brain, according to the report in the current issue of The Journal of Neuroscience.
“This is first time anyone has shown, in vivo, a decrease in serotonin binding in panic disorder patients. Eventually, this work could lead to new more selective pharmacological treatments that would specifically target this receptor,” says Michael Davis, PhD, of Emory University, who studies anxiety disorders. “Clinical studies like this are extremely important for guiding basic research in animals to understand more fully the role of these receptors in anxiety.”
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 a genetic component.
In the study, Neumeister and his colleagues used PET scans to visualize serotonin 5-HT1A receptors in the brains of 16 panic disorder patients – seven of whom also suffered from major depression – and 15 matched healthy controls. In the panic disorder patients, including those who also had depression, receptors were reduced by an average of nearly a third in the anterior cingulate in the front middle part of the brain, the posterior cingulate, in the rear middle part of the brain, and in the raphe, in the midbrain.
Reduced expression of the receptor “may be a source of vulnerability in humans, and that abnormal function of these receptors appears to specifically impact the cortical circuitry involved in the regulation of anxiety,” the authors say.
Neumeister’s co-authors include Wayne Drevets, Earle Bain, Allison Nugent, Richard Carson, Omer Bonne, David Luckenbaugh, William Eckelman, Peter Herscovitch, and Dennis Charney. The Journal of Neuroscience is published by the Society for Neuroscience, an organization of more than 34,000 basic scientists and clinicians who study the brain and nervous system. Neumeister can be reached through Jules Asher at NIMH at (301) 443-4536.