Deletion of the serotonin transporter (SERT) in mice produced an alteration in brain 5HT homeostasis, decreased tissue concentrations of 5HT, and an increase in anxiety-related behaviors (EPM, light/dark box test) that was more pronounced in females than males.32

Deletion of the gene for the 5HT1A receptor produced an 'anxious' phenotype in a variety of anxiety models. In addition to this anxiogenic profile, 5HT1A knockout mice also showed increased autonomic activity (i.e., elevated body temperature, tachycardia) in response to stress, changes that are similar to those seen in humans with anxiety or stress disorders.

Deletion of the 5HT1B receptor gene has been associated with increased aggression. The presence of an anxiety-related phenotype in these mice is equivocal as increased, decreased, or unchanged anxiety levels have been reported in the EPM and light/dark box. 5HT1B knockouts exhibited reduced anxiety in the EPM and the novel exploration and novelty suppressed feeding tasks but showed no difference in the light/dark box test.33

Mutant 5HT2C receptor mice have a reduced anxiety phenotype, perhaps consistent with the findings that show an anxiolytic effect of 5HT2C antagonists in animals.34 Experiments with mice lacking the gene for the 5HT5A receptor suggest that this receptor may modulate exploratory behavior rather than anxiety per se.35

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