Brain potential signs of slowed stimulus processing following cholecystokinin in Parkinson's disease
- Cite this article as:
- Smolnik, R., Fischer, S., Hagenah, J. et al. Psychopharmacology (2002) 161: 70. doi:10.1007/s00213-002-1010-9
Rationale: Cholecystokinin (CCK) is a neuropeptide which is colocalized with dopamine (DA) in neurons of the mesolimbic-frontocortical and nigrostriatal DA system. In animals CCK enhances DA activity in these systems. Objectives: The present study examined the effects of a single intranasal administration of CCK-8 on auditory brain potential (AEP) signs of cognitive processing and on motor performance in patients with Parkinson's disease (PD), known to originate from degeneration of DA neurons primarily in the nigrostriatal DA system. Methods: Thirteen PD patients were examined after medication withdrawal, on two occasions after administration of placebo and 25 µg CCK-8, and compared with healthy controls matched for age and sex. AEPs were recorded while subjects performed an attention task (oddball paradigm). Results: In the placebo condition, AEPs in the PD patients did not show marked alteration but were rather comparable to those in the controls. In healthy controls, CCK-8 enhanced the P3 complex (P<0.05) and shortened latencies of the N2 and P3 components of the AEP evoked by task relevant target stimuli (P<0.05). Contrary to expectations, in PD patients these AEP components were distinctly delayed after CCK–8 (P<0.05). Motor performance was not changed by CCK-8 in PD patients or in controls. Conclusion: Data indicate a deleterious rather than beneficial effect of CCK on cognitive processing in PD patients that might result from a prevailing effect of the neuropeptide on transmitter systems (e.g. GABAergic) other than the DA system.