- Contains a disruption of the serotonin transporter (5-HTT) gene (Slc6a4).
- Marked increases in brain extracellular fluid together with reduced serotonin concentrations in the brain and peripheral organs and desensitization of some subsets of serotonin receptors.
- Altered responses to substances of abuse (e.g., ecstasy, cocaine)
- Displays normal embryonic development and growth as well as normal fertility and viability.
- Useful model to study mechanisms of action of drugs used for treatment of serotonin-related disorders and drugs of abuse.
Genetic Background: C57BL/6
Origin: The Serotonin Transporter knockout model was developed by Bengel et al. in the laboratory of Dennis Murphy of NIHMH by disrupting the Slc6a4 gene via homologous recombination in 129 R1 embryonic stem cells. Targeted ES cells were injected into C57BL/6J blastocyts. The mice were then backcrossed nine generations (N9) to a C57BL/6J inbred background. Taconic received stock in February 2001. The mice were derived by embryo transfer and maintained by homozygous breeding.
Bengel D., Murphy DL, Andrews AM, Wichems CH, Feltner D, Heils A, Mossner R, Westphal H, Lesch K-P, (1998) Altered Brain Serotonin Homeostasis and Locomotor Insensitivity to 3,4-Methylenedioxymethamphetamine (“Ecstasy”) in Serotonin Transporter-Deficient Mice
. Mol Pharmacol, 53:649-655