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22 The administration of reserpine to rodents has been suggested as a 23 pharmacological model of Parkinson disease (PD) based on the effects 24 of this monoamine-depleting agent on motor activity. Reserpine 25 interferes with the storage of monoamines in intracellular vesicles, 26 causing monoamine depletion in nerve terminals and transient 27 hypolocomotion and muscular rigidity, depending on the dose 28 (Colpaert 1987; Gerlach and Riederer, 1996). However, it is important 29 to note that the use of reserpine treatment as a model of PD presents 30 some limitations due to the fact that the drug does not induce 31 nigrostriatal pathway degeneration. 32 Apart from the motor disturbance, other symptoms are presented 33 by parkinsonian patients, including expressive cognitive deficits 34 (Dubois et al., 1994; Shults, 2003; Lauterbach, 2004; Owen, 2004; 35 Matsui et al., 2006). There is evidence that cognitive symptoms found 36 in PD are related to executive dysfunction, in particular to working 37 memory, but also planning and problem solving (Karel et al., 1996; 38 Owen et al., 1998; Cox et al., 2002; Cools et al., 2002; Higginson et al., 39 2003; Lewis et al., 2003; 2005; Monchi et al., 2007; Nieoullon, 2002; 40 Zgaljardic et al., 2004). Further, patients with Parkinson disease 41 present alterations in stimulus response associations (Shohamy et al., 42 2005; Nagy et al., 2007), implicit learning (Schneider et al., 2003; 43 Castner et al., 2007); feed-back based learning (Schimitt-Eliassen 44 et al., 2007) reversal learning (Cools et al., 2007) and spatial memory 45 (Pillon et al., 1996, 1997a, b; Giraudo et al., 1997). In this respect, 46 studies …