TABLE 3. Rapid dopamine depletion by AMPT paradoxically exacerbated GluA1 locomotor hyperactivity.

Vehicle treated KO traveled significantly farther than WT, whereas AMPT treatment produced a further increase in KO but had no effect in WT (&&p<.01 vs. WT/same treatment; #p<.05 vs. KO/vehicle) (n=12-16/genotype/treatment). AMPT treatment decreased striatal tissue levels (ng/g tissue) of dopamine, DOPAC, HVA, and 3-MT, irrespective of genotype (n=10-11/genotype/treatment) (**p<0.01). AMPT treatment significantly increased striatal serotonin regardless of genotype (††p<0.01), but increased 5-HIAA only in KO (#p<.05 vs. KO/vehicle). Norepinephrine content was unaffected by treatment or genotype. Data are Means ±SEM.

	WT		KO
	VEH	AMPT	VEH	AMPT
Novel open field
Total distance traveled (m)	61.6 ±5.9	49.2 ±4.2	115.2 ±11.7&&	155.9±15.4&&#
Striatal monoamine levels
Dopamine**	3555.8 ±599.1	937.5 ±281.9	2797.6 ±461.5	1235.1 ±285.8
DOPAC**	344.7 ±32.9	80.8 ±15.3	270.8 ±33.9	84.8 ±10.1
HVA**	649.6 ±76.6	196.2 ±26.4	561.4 ±79.4	241.3 ±34.3
3-MT**	123.8 ±17.1	31.9 ±10.7	93.2 ±18.1	50.2 ±13.2
Serotonin††	1080.6 ±46.9	1202.3 ±65.3	1054.7 ±64.9	1343.2 ±86.4
5-HIAA	657.8 ±49.2	557.7 ±48.3	540.8 ±41.5	720.8 ±65.9#
Norepinephrine	565.6 ±55.0	569.5 ±55.2	685.4 ±58.6	578.9 ±48.6