Psychopharmacology · 13 authors, 6 centres
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This preclinical study administered MAM-2201 and its analogue AM-2201 to mice to compare their effects on motor, sensorimotor, and cognitive functions. The central result was that MAM-2201 induced impairments in motor, sensorimotor, sensory gating (prepulse inhibition), and working memory functions via a CB1 receptor-mediated mechanism.
The study used in vitro competition binding to assess affinity for murine and human CB1 and CB2 receptors and in vivo behavioral testing in CD-1 male mice. In vitro, both MAM-2201 and AM-2201 showed nanomolar affinity for CB1 and CB2 receptors, with a preference for CB1. In vivo, MAM-2201 administration impaired visual, acoustic, and tactile sensorimotor responses, spontaneous locomotor activity, prepulse inhibition (a measure of sensory gating), and both short- and long-term working memory. The sensorimotor impairments were fully prevented by pretreatment with the CB1 receptor antagonist AM-251, indicating a CB1 receptor-mediated mechanism. The comparison showed AM-2201 also caused working memory deficits. The findings suggest potential public health risks related to impaired driving and workplace performance.
