Unaltered striatal A2AR responses in hMT mice. (a) The A2AR agonist CGS21680 suppressed spontaneous locomotion in all genotypes. Animals were injected i.p. with vehicle (NT n = 27, hWT n = 29, hMT n = 13), CGS21680 0.25 mg/kg (n = 8, per genotype) or CGS21680 0.5 mg/kg (n = 8, per genotype). Locomotion is expressed as manually counted number of sector crossing (mean SEM) over a 30 min test. (b) The A2AR antagonist KW6002 stimulated motor activity in all tested groups. Mice were injected i.p. with vehicle (n = 13, per genotype), KW6002 1.5 mg/kg (NT n = 8, hWT n = 7, hMT n = 8) or KW6002 3 mg/kg (n = 8, per genotype). Locomotion is expressed as manually counted number of sector crossing (mean ± SEM) over 60′ test, after 60′ habituation. Genotypes and treatments are as indicated vehicle: veh, CGS21680: CGS, KW6002: KW. ## p < 0.01, ### p < 0.0001 compared with vehicle group, within genotype. (c) Sample EPSCs showing that paired-pulse ratio (PPR, 50 ms interstimulus interval) was unaffected by bath-application of SCH 58261 (grey traces) both in hWT and hMT mice. Right. Summary plot of the changes in PPR in the three genotypes. (d). Superimposed traces showing the lack of effect of SCH 58261 on the two synaptic components, NMDA and AMPA, recorded at +40 mV and −60 mV, respectively, in hWT and hMT mice. Right. Summary plot of the effect of SCH 58261 on AMPA/NMDA ratio. e. Representative traces show that SCH 58261 does not modify the inward current induced by focal application of both AMPA (e) or NMDA (f) in both hWT and hMT mice in control conditions and in the presence of SCH 58261 (grey traces).