However, these mice demonstrate markedly increased locomotor responses to amphetamine compared with WT animals.

We report that M1 deficiency leads to elevated dopaminergic transmission in the striatum and significantly increased locomotor activity.

In addition, mice lacking MCH have a phenotype of increased locomotor activity, an effect also seen in both strains.

Instead, FGF1-Tek mice display increased locomotor activity that likely promotes the utilization of dietary fatty acids before they can accumulate in adipose and liver.

Tph2 mutant mice, completely devoid of 5-HT synthesis in brain, displayed accelerated fear memory formation and increased locomotor responses to foot shock.