The Columbia University scientists found that mice lacking a serotonin receptor shortly after birth were abnormally anxious when they were grown up regardless of whether the receptor was present or not during adulthood.

They believe that postnatal developmental processes may help to establish adult anxiety-like behavior and that the postnatal period is a critical time for the establishment of lifelong anxiety behavior.

In the latest edition of Nature, the team describe how they controlled the serotonin1A receptor in a group of mice by using the antibiotic doxycycline. The gene could be switched off simply by feeding mice the antibiotic.

For one group of mice the receptors were switched off throughout the brain during gestation.

A second group of mice, in which serotonin1A receptors were only present in the forebrain, was also studied. In this group the receptors were switched off between 10 and 12 weeks of age.

The mice lacking the serotonin receptor throughout the brain from birth showed pronounced anxiety-like behavior. In comparison, the group with forebrain receptors that were switched off during their juvenile years did not display such behavior.

Furthermore, selective restoration of forebrain serotonin receptors in the mice lacking serotonin throughout the brain restored normal behavior.

The researchers concluded that serotonin1A receptors in the forebrain regulate anxiety whereas receptors in the hindbrain do not seem to be directly involved.

The researchers believe that forebrain serotonin1A receptors are needed during the development of newborns to modulate the predisposition to anxiety-like behavior, but are no longer critical during adult life.

Writing in Nature the researchers said, “We note that in humans chronic treatment with direct serotonin1A receptor agonists…is required for therapeutic efficacy, raising the possibility that, both during development and in adulthood, activation of the serotonin1A receptors can elicit long-term plastic changes that decrease anxiety-like behavior.”

“The discovery that anxiety is linked to the need for serotonin 1A receptors in a specific brain region at a particular period of development adds a new layer of understanding of serotonin’s function,” Solomon H Snyder of Baltimore’s Johns Hopkins University School of Medicine said in an accompanying commentary.

Source: Nature, March 2002

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