“…They also exhibit modest agonist properties at 5-HT 1A receptors (Newman-Tancredi et al, 1998), so interpretation of their effects is complex. Any of these non-5-HT 2A actions could be responsible for the loss of antiparkinsonian (Lejeune et al, 1997); E max , 101% (Cornfield et al, 1991) Buspirone Reduces AIMs, impairs rotarod performance, this latter action may reflect loss of antiparkinsonian benefit (Dekundy et al, 2007) Reduces dyskinesia, but worsens parkinsonism (Ludwig et al, 1986;Bonifati et al, 1994) K i , 20 nM (Hamik et al, 1990); E max , 22% (Dupuis et al, 1999) Sarizotan Reduces AIMs (Marin et al, 2009) Reduces dyskinesia and L-DOPA antiparkinsonian benefit at high dose (Gregoire et al, 2009) Reduces dyskinesia (phase II) (Olanow et al, 2004), reduces dyskinesia compared with baseline, but not compared with placebo (phase III) (Goetz et al, 2008), no dyskinesia reduction and worsening of parkinsonism (phase III) (Goetz et al, 2007) K i , 2.2 nM (Newman-Tancredi et al, 2005); E max , 100% (Bartoszyk et al, 2004) Tandospirone Reduces dyskinesia, but worsens parkinsonism (Kannari et al, 2002) K i , 27 nM (Hamik et al, 1990); E max , 67% (Tamaoki et al, 2007) Anatomically Selective Therapies for Parkinson's Disease efficacy, and it could be argued that even the antidyskinetic actions of these compounds have little to do with 5-HT 2A antagonism. However, a PET study performed in schizophrenic patients demonstrated that at doses used to treat PD motor and nonmotor complications clozapine leads to greater 5-HT 2 than D 2 -like receptor occupancy (Nordström et al, 1995).…”