Spine pruning drives antipsychotic-sensitive locomotion via circuit control of striatal dopamine

This study identifies a mechanism linking loss of Arp2/3 to the progressive formation of shaft excitatory synaptic contacts. This leads to enhanced cortical excitation, striatal hyperdopaminergia and antipsychotic-responsive psychomotor agitation. This illustrates how diverse pathologies may converge downstream of spine actin disturbances to drive psychomotor behaviors.