Fig 1.
Schematic illustrations of placements.
(A) A coronal mouse brain section showing five representative guide cannula placements (illustrated by vertical lines) aiming at the third ventricle (icv) [25]. In addition, a slice from mouse brain show one representative placement of a guide cannula in the third ventricle (B) A coronal mouse brain section showing six representative probe or guide cannula placements (illustrated by vertical lines) in the nucleus accumbens (NAc) shell [25]. Moreover, a slice from a mouse brain shows one representative placement in the NAc shell. For each brain section only a few representative placements are illustrated, but all other placements targeted the third ventricle or were within the NAc shell. Placements outside these areas were not included in the statistical analysis. The number given in the brain section indicates millimeters anterior (+) or posterior (-) from bregma.
Fig 2.
Central (1 μg, icv) administration of NMU attenuates amphetamine-induced locomotor stimulation, accumbal dopamine release and expression of conditioned place preference in mice.
(A) Amphetamine-induced (2 mg/kg, ip) locomotor stimulation was blocked by a central injection of NMU (1 μg, icv) at time point 15–35 minutes. Central NMU administration had no effect per se on locomotor activity. (B) NMU (1 μg, icv) attenuated amphetamine (2 mg/kg, ip) induced increase in accumbal dopamine release at time point 40–80 minutes. (C) Central NMU (1 μg, icv, Amph-NMU) administration prevented the amphetamine (2 mg/kg, Amph-Veh) induced expression of conditioned place preference (CPP). Data are presented as mean ± SEM (*P<0.05, **P<0.01, ***P<0.001 for Veh-Veh versus Veh-Amph and # P<0.05, ## P<0.01, ### P<0.001 for Veh-Amph versus NMU-Amph).
Fig 3.
Central (0.3 μg, icv) administration of NMU reduces amphetamine-induced locomotor stimulation in mice.
Amphetamine-induced (2 mg/kg, ip) locomotor stimulation was reduced, but not blocked, by a central injection of a lower does of NMU (0.3 μg, icv). Central administration of this lower dose of NMU had no effect per se on locomotor activity. Data are presented as mean ± SEM (n.s. P>0.05, *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 compared to vehicle-vehicle treatment).
Fig 4.
Accumbal administration of NMU attenuates amphetamine-induced locomotor stimulation, but does not affect the expression of conditioned place preference in mice.
(A) Amphetamine-induced (2 mg/kg, ip) locomotor stimulation was attenuated by an accumbal injection of NMU (62.5 ng per side). Accumbal NMU administration had no effect per se on locomotor activity. (B) Accumbal NMU (62.5 ng per side, Amph-NMU) administration did not attenuate amphetamine-induced (2 mg/kg, ip, Amph-Veh) expression of CPP in mice. Data are presented as mean ± SEM (n.s. P>0.05, *P<0.05).