Figure 5.
A developmental deficit in γ2 subunit-containing GABAARs results in greater inhibition in two behavioral assays sensitive to antidepressant drug treatment. The three different mouse lines (γ2+/−, Emx1Cre × fγ2/+, and CaMKIICre2834 × fγ2/+) together with their respective littermate controls (wt and fγ2/+ mice, respectively) were subjected to the modified forced swim (Lucki, 1997) (a–c) and novelty-suppressed feeding (Santarelli et al., 2003) (d–f) tests. a, In the forced swim test, γ2+/− mice started floating significantly earlier and spent more time immobile than wt controls (U = 13.0 and 20.0, respectively; p < 0.05; n = 9 per genotype). b, Tested under the same conditions, Emx1Cre × fγ2/+ mice did not differ significantly from fγ2/+ with respect to mean time to first immobility (U = 26) but exhibited an increase in the mean time spent immobile compared with controls (U = 2.5; n = 6–14; p < 0.001). c, CaMKIICre2834 × fγ2/+ mice were indistinguishable from fγ2/+ littermates for both parameters. d, In the novelty-suppressed feeding test, γ2+/− mice showed a heightened mean latency to initiate feeding compared with wt (U = 19; p < 0.05; n = 9 per genotype). e, Likewise, the mean latency to initiate feeding was significantly increased in Emx1Cre × fγ2/+ compared with controls (U = 3.0; n = 6–14; p < 0.001). f, In the novelty-suppressed feeding test, CaMKIICre2834 × fγ2/+ mice were indistinguishable from fγ2/+ littermate controls (U > 33; n = 8–12 per genotype). Values represent group means ± SEM.