Introduction

The research on timing and time perception conducted over the years in our laboratory has been driven by the assumption that a psychophysical model such as scalar expectancy theory (SET) would provide us with the advantages of a conceptual framework and the appropriate analytic tools to guide the search for the neurobiological mechanisms of the interval timing. We generated a body of data about the performance of patients with damage to different neural systems on the peak-interval (PI) timing production task, which yielded results amenable to analysis of timing accuracy, variability, and the scalar property using the SET framework (Malapani et al., 1998a, 1998b; Rakitin et al., 1998). A variety of patterns of temporal data generated by this procedure in animals have been found to be diagnostic of the level where a behavioral, pharmacological, or physiological manipulation acts in an information-processing model of interval timing (Gibbon and Church, 1984; Gibbon et al., 1984; Hinton and Meck, 1997; Meck, 1996). Our own findings argued strongly in favor of this approach for clinical research. We showed that simultaneous consideration of changes in both accuracy and variability of timing systems clearly distinguished deficits of temporal behavior resulting from damage to distinct brain regions (Malapani and Fairhurst, 2002).

However, there are major psychophysical findings of timing research that still remain poorly understood (Malapani and Fairhurst, 2002). More importantly, our level of understanding of both the neural basis of timing and the psychophysics of timing now exceeds our understanding of the connection between these two largely independent domains of investigation (Malapani et al., in press). As John Gibbon stated in his most recent paper, all these issues await for new theoretical developments in modeling timing and time perception (Gibbon and Malapani, 2002). Recent attempts made in that direction are quite promising (Matell and Meck, 2000, in press). Although the computations implemented by these studies appear more biologically plausible in translating psychophysical properties of timing systems, such as the scalar property, they do not reproduce the timing errors that have come to light in studies of Parkinson's disease (PD) patients.

In this chapter, we first describe the effects of dopamine (DA) depletion on timing performance previously reported in PD that current timing theories, including SET, cannot account for. We then discuss the way those findings force a rethinking of the theory that led us to propose a new computational model attempting to account for at least some of the timing errors seen in PD. This new model, although limited, might be an important contribution in the future search of valuable connections between neurobiology and psychology of timing behavior. The last part of this chapter contrasts the effects of DA to deep brain stimulation (DBS) in parkinsonian timing, which seem to challenge both functional anatomy and theoretical accounts of the basal ganglia involvement in timing and time representation. The questions we raise will be answered by future research.

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