. Author manuscript; available in PMC: 2009 Sep 18.

Published in final edited form as: Curr Chem Genomics. 2008 Jan 1;2:62–75. doi: 10.2174/1875397300802010062

Table 2. Evaluation of Genetic Animal Models of OCD.

Genetic Model	Face Validity^*	CSTC Circuit Expression^ˆ	CSTC Synaptic Dysfunction	Response to SSRIs
D1CT Tg	+++	++	++	nd
Hoxb8 mutant	+++	+++	nd	nd
5-HT_2C null	+	+	nd	nd
ArKO	++	?	nd	nd
DAT KD	+	+++	+++	nd
SAPAP3 null	+++	+++	+++	++

D1CT Tg, transgenic mouse line in which neuropotentiating cholera toxin is expressed under the D1-type dopamine receptor promoter elements; Hoxb8 mutant, homozygous loss-of-function for mammalian transcription factor Hoxb8; 5-HT_2C null, null mutant mouse for the 5-HT_2C subtype of the serotonin receptor; ArKO (for aromatase knock-out), estrogen deficient mouse line resulting from elimination of aromatase expression; DAT KD, dopamine transporter knock-down mice with DAT levels reduced to 10% of wild-type values; SAPAP3 null, null mutant mouse for the postsynaptic scaffolding protein SAPAP3.

Note that face validity incorporates both behavioral similarity AND specificity.

^ˆ

CSTC circuit expression refers to the extent to which the gene or Tg is expressed in these brain regions.

nd - not demonstrated.