Recent evidence suggests that psychedelic drugs can exert beneficial effects on anxiety, depression, and ethanol and nicotine abuse in humans. However, the hallucinogenic side effects of psychedelics often preclude their clinical use. Lysergic acid diethylamide (LSD) is a prototypical hallucinogen and its psychedelic actions are exerted through the 5HT2A serotonin receptor (5HT2AR). 5HT2AR activation stimulates Gq and arrestin (Arr) mediated signaling. To separate effects of these signaling modes, we have used Arr1 and Arr2 mice. We find that LSD stimulates motor activities to similar extents in WT and Arr1 KO mice, with non-significant effects in Arr2 KOs. LSD robustly stimulates many surrogates of psychedelic drug actions including head twitches, grooming, retrograde walking, and nose poking in WT and Arr1 KO animals. In contrast, LSD only slightly stimulates head twitches in Arr2 KO mice, without effects on retrograde walking or nose poking. The 5HT2AR antagonist MDL100907 (MDL) blocks these LSD effects. LSD also disrupts prepulse inhibition (PPI) in WT and Arr1 KOs. PPI is unaffected in Arr2 KOs. MDL restores PPI in WT mice, but this antagonist is without effect and haloperidol is required in Arr1 KOs. LSD produces a biphasic body-temperature response in WT mice, a monophasic response in Arr1 KOs, and is without effect in Arr2 mutants. Both MDL and the 5HT1AR antagonist, WAY100635 (WAY), block the effects of LSD on body temperatures in WT mice, whereas WAY is effective in Arr1 KOs. Collectively, these results reveal that LSD produces diverse behavioral effects through Arr1 and Arr2, and that the psychedelic drug-like actions of LSD appear to require Arr2.