GIT1 regulates synaptic structural plasticity underlying learning
Fig 2
Amphetamine-induced locomotor activity in GIT1 deficient mice.
GIT1 WT (black circle) and GIT1 KO (open square) mice on a mixed genetic background were habituated to the locomotor chamber for 60 min prior to amphetamine injection. A) GIT1 WT (n = 9) and GIT1 KO (n = 8) mice were injected with 4mg/kg amphetamine in their active (dark) phase, and activity is shown in 5 min windows. B) Drug-induced locomotor activity (dark phase, 4mg/kg amphetamine) was totaled over 1h and 2h following injection. No difference between WT and KO. C) GIT1 WT (n = 6) and GIT1 KO (n = 5) mice were injected with 4mg/kg amphetamine in their inactive (light) phase. D) Drug-induced locomotor activity (light phase, 4mg/kg amphetamine) was totaled over 1h and 2h following injection. No difference. E) GIT1 WT (n = 8), GIT1 KO (n = 7) and GIT1 heterozygote (Het, n = 5) mice were injected with 2mg/kg amphetamine in their inactive (light) phase. F) Drug-induced locomotor activity (light phase, 2mg/kg amphetamine) was totaled over 1h and 2h following injection. No difference. p<0.001 in a two-way repeated measures ANOVA between genotypes over time; * p<0.05, ** p<0.01, *** p<0.001 within time using a Holm-Sidak post-hoc test.