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Some antipsychotic drugs may be missing their mark
January 02, 2008COLUMBUS, Ohio - Drugs that treat depression, schizophrenia and other psychotic conditions and that target a particular protein on brain cells might not be triggering the most appropriate response in those cells, new research suggests.
The study by researchers at The Ohio State University Medical Center examined the serotonin 2A receptor, a protein on brain cells sensitive to the neurotransmitter serotonin.
This study examined the early chemical events that happen inside neurons when the 2A receptor is stimulated by serotonin and by a synthetic hallucinogenic agent that is thought to mimic serotonin.
The findings, published online in the early edition of the Proceedings of the National Academy of Sciences with an accompanying editorial, show that although both compounds combine with and activate this receptor, they trigger different chemical pathways inside the neuron.
Researchers say that the work could have important implications for the development of drugs that affect the serotonin 2A receptor, a key target in the treatment of several important mental disorders.
"This new insight into how serotonin and a hallucinogenic drug affect this serotonin receptor could lead to changes in how new drugs are screened and developed for depression, schizophrenia and other neuropsychiatric disorders," says study leader Laura M. Bohn, an associate professor of pharmacology and psychiatry.
Currently, it is thought that when serotonin binds with the receptor, it sends a signal that activates molecules inside the cell called G proteins.
This study shows, however, that the receptor responds to serotonin by also activating a protein called beta-arrestin inside the cell. The synthetic hallucinogen, on the other hand, causes the receptor to activate only the G proteins. The hallucinogen does not seem to use beta-arrestins to cause its effects.
For this study, Bohn and her colleagues used laboratory-grown cells and a strain of mice that lacked beta-arrestin. The hallucinogen was a hallucinogenic amphetamine called DOI.
When the researchers injected normal (i.e., control) and experimental mice with DOI, both groups showed a head-twitch behavior, a characteristic response in mice to hallucinogens.
But when the mice were given high doses of serotonin, which typically also causes the head-twitch behavior, the behavior occurred in the control animals only, and not in the mice lacking beta-arrestin.
"That demonstrates that the signal for serotonin requires beta-arrestin for that biological effect," Bohn says. "The synthetic hallucinogen, on the other hand, induces the head-twitch behavior whether beta-arrestin is present or not.
"Overall, our findings suggest that the screening of agents intended to be serotonin mimics must also determine if the agent signals through beta-arrestin," Bohn says. "That isn't done now."
Ohio State University
The findings, published online in the early edition of the Proceedings of the National Academy of Sciences with an accompanying editorial, show that although both compounds combine with and activate this receptor, they trigger different chemical pathways inside the neuron.
Researchers say that the work could have important implications for the development of drugs that affect the serotonin 2A receptor, a key target in the treatment of several important mental disorders.
"This new insight into how serotonin and a hallucinogenic drug affect this serotonin receptor could lead to changes in how new drugs are screened and developed for depression, schizophrenia and other neuropsychiatric disorders," says study leader Laura M. Bohn, an associate professor of pharmacology and psychiatry.
Currently, it is thought that when serotonin binds with the receptor, it sends a signal that activates molecules inside the cell called G proteins.
This study shows, however, that the receptor responds to serotonin by also activating a protein called beta-arrestin inside the cell. The synthetic hallucinogen, on the other hand, causes the receptor to activate only the G proteins. The hallucinogen does not seem to use beta-arrestins to cause its effects.
For this study, Bohn and her colleagues used laboratory-grown cells and a strain of mice that lacked beta-arrestin. The hallucinogen was a hallucinogenic amphetamine called DOI.
When the researchers injected normal (i.e., control) and experimental mice with DOI, both groups showed a head-twitch behavior, a characteristic response in mice to hallucinogens.
But when the mice were given high doses of serotonin, which typically also causes the head-twitch behavior, the behavior occurred in the control animals only, and not in the mice lacking beta-arrestin.
"That demonstrates that the signal for serotonin requires beta-arrestin for that biological effect," Bohn says. "The synthetic hallucinogen, on the other hand, induces the head-twitch behavior whether beta-arrestin is present or not.
"Overall, our findings suggest that the screening of agents intended to be serotonin mimics must also determine if the agent signals through beta-arrestin," Bohn says. "That isn't done now."
Ohio State University
Study points to new uses, unexpected side effects of already-existing drugs
Scientists at the University of North Carolina at Chapel Hill School of Medicine and the University of California, San Francisco have developed and experimentally tested a technique to predict new target diseases for existing drugs.
Spiritual effects of hallucinogens persist, Johns Hopkins researchers report
In a follow-up to research showing that psilocybin, a substance contained in "sacred mushrooms," produces substantial spiritual effects, a Johns Hopkins team reports that those beneficial effects appear to last more than a year.
Hopkins scientists show hallucinogen in mushrooms creates universal 'mystical' experience
Using unusually rigorous scientific conditions and measures, Johns Hopkins researchers have shown that the active agent in "sacred mushrooms" can induce mystical/spiritual experiences descriptively identical to spontaneous ones people have reported for centuries.
When smoking was believed to cure cancer! [National No Smoking Day: 12 March 2003]
Smoking was believed to provide a cure for cancer! - That's one of the surprising facts arising from a detailed study into tobacco use by a University of Leicester academic. Dr Jason Hughes has moved beyond his study into the biological addiction to smoking and instead examines how social and personal understandings of smoking crucially affect the way people experience it. Dr Hughes, a Lecturer in the University's Centre for Labour Market Studies, has a particular interest in sociology and uses this to address the question of why people smoke. He said: "I have previously examined the diverse sociological and cultural processes that have compelled people to smoke since the practice was fi
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