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RecentstudiesdemonstratedthatactivationoftheGABABreceptor,eitherbymeansoforthostericagonistsorpositiveallostericmodulators(PAMs),inhibiteddifferentnicotine-relatedbehaviors,includingintravenousself-administrationandconditionedplaceprefer-ence,inrodents.Thepresentstudyinvestigatedwhethertheanti-nicotineeffectsoftheGABABreceptoragonist,baclofen,andGABABPAMs,CGP7930,andGS39783,extendtonicotinestimulanteffects.Tothisend,CD1micewereinitiallytreatedwithbaclofen(0,1.25,and2.5mg/kg,i.p.),CGP7930(0,25,and50mg/kg,i.g.),orGS39783(0,25,and50mg/kg,i.g.),thentreatedwithnicotine(0and0.05mg/kg,s.c.),andfinallyexposedtoanautomatedapparatusforrecordingoflocomotoractivity.Pretreatmentwithdosesofbaclofen,CGP7930,orGS39783thatdidnotalterlocomotoractivitywhengivenwithnico-tinevehiclefullypreventedhyperlocomotioninducedby0.05mg/kgnicotine.ThesedataextendtonicotinestimulanteffectsthecapacityofbaclofenandGABABPAMstoblockthereinforcing,motivational,andrewardingpropertiesofnicotine.ThesedatastrengthenthehypothesisthatactivationoftheGABABreceptormayrepresentapotentiallyuseful,anti-smokingtherapeuticstrategy

Activation of the GABAB Receptor Prevents Nicotine-Induced Locomotor Stimulation in Mice