The depressed patients treated with the placebo showed no benefit.
In a report published this summer in the journal Molecular Psychiatry, the USF researchers suggest that many newer, more selective antidepressants such as Prozac work, in part, by inactivating nicotine receptors in the brain. These receptors appear to be overstimulated by the biochemical messenger acetylcholine in patients who are depressed.
The most common current explanation for how antidepressants work is by boosting levels of serotonin, a brain biochemical that is low in people with depression.
"Our preliminary findings with mecamylamine suggest that another way antidepressants may improve depressed moods is by blocking acetylcholine's excess activation of nicotine receptors," said investigator Paul R. Sanberg, PhD, DSc, professor and director of the USF Neuroscience Program.
"It allows us to explore a new class of drugs for neuropsychiatric disorders," said investigator Archie Silver, MD, director of the USF Center for Infant and Child Development.
The USF research team recently started a controlled study of mecamylamine in children and adolescents with bipolar disorder, also known as manic depression. This latest study is funded in part by the Stanley Medical Research Institute.
Other authors of study in Depression and Anxiety were Kathy Sheehan, PhD; and David Sheehan, MD.
The study was supported in part by a grant from the USF High-Tech Corridor Project. The researchers got mecamylamine through Layton BioScience, Inc., a California biotechnology firm that owned rights to the medication at the time of the study.
Mecamylamine (Inversine™) is now owned and marketed by Targacept, a Salem, NC pharmaceutica
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Contact: Anne DeLotto Baier
abaier@hsc.usf.edu
813-974-3300
University of South Florida Health
10-Dec-2002