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FIGURE 12.7 Dopamine, clock speed, and attention sharing. (A) Relation between time processing, attention sharing, and general processing. Data reviewed here suggest that dopaminergic drugs affect the accumulation of temporal units by two independent processes: changes in the speed of the pacemaker and changes in allocation of attentional resources. (B) A possible implementation of an active decay mechanism controlled by attention sharing. Lower left panel: The subjective time stored in the accumulator decays during the presentation of the gap at a rate proportional to the attention paid to these events. The salience, content, and similarity with the ITI affect the rate of decay. Lower right panel: Dopaminergic agonists increase the rate of the pacemaker (increase the slope of the accumulation line) and increase the rate of decay during the gap by promoting a reduction in the attentional resources allocated to the timing component of the task. Horizontal broken line, criterion interval; broken arrows, peak times. The diagrams under the graphs depict the to-be-timed stimulus in PI trials and in trials with low-intensity and high-intensity gaps.

FIGURE 12.7 Dopamine, clock speed, and attention sharing. (A) Relation between time processing, attention sharing, and general processing. Data reviewed here suggest that dopaminergic drugs affect the accumulation of temporal units by two independent processes: changes in the speed of the pacemaker and changes in allocation of attentional resources. (B) A possible implementation of an active decay mechanism controlled by attention sharing. Lower left panel: The subjective time stored in the accumulator decays during the presentation of the gap at a rate proportional to the attention paid to these events. The salience, content, and similarity with the ITI affect the rate of decay. Lower right panel: Dopaminergic agonists increase the rate of the pacemaker (increase the slope of the accumulation line) and increase the rate of decay during the gap by promoting a reduction in the attentional resources allocated to the timing component of the task. Horizontal broken line, criterion interval; broken arrows, peak times. The diagrams under the graphs depict the to-be-timed stimulus in PI trials and in trials with low-intensity and high-intensity gaps.

time in opposite directions in PI trials and gap trials (right panel of Figure 12.3), suggesting that the attentional effects of these drugs are not due to their possible effects on the speed of the internal clock (Maricq et al., 1981; but see Santi et al., 1995). For example, dopaminergic drugs might affect active decay of accumulated time. For example, the right lower panel of Figure 12.7 shows that MAP might (a) increase the rate of the pacemaker, and (b) facilitate the decay of accumulated time during interrupting events by facilitating reallocation of attentional resources away from the timing component of the task. In accord with data discussed here, MAP would (a) produce a leftward shift in PI trials (left panel of Figure 12.3), and (b) promote a resetting of timing after the gap (right panel of Figure 12.3).

The clock and attention-sharing patterns of dopaminergic drugs might be related to the affinity of dopaminergic drugs to the D1 and D2 dopamine receptors, respectively (see Stanford and Santi, 1998; Meck, 1986). In this scenario, drugs that activate both receptors, such as amphetamine, are expected to determine both effects, while drugs that selectively affect the D2 dopamine receptor, such as quinpirole, are expected to determine only the attentional effect (Frederick and Allen, 1996; Stanford and Santi, 1998; but see Castner et al., 2000; Müller et al., 1998). Indeed, in our experiments MAP shifted the peak time in opposite directions in probe trials with or without gaps, indicative of both clock and attentional effects, while HAL shifted the peak time significantly in trials with gaps, but only marginally in trials without gaps, indicative of a predominantly attentional effect rather than a clock speed effect (see Figure 12.3). On the other hand, results might be due to the activation of the noradrenergic (Al-Zahrani et al., 1998) or serotonergic (Chiang et al., 1999) systems. Further pharmacological, neurophysiological, and genetic manipulations using the behavioral paradigms described here will help elucidate the biological substrates of the attentional mechanisms of interval timing.

12.5.3 Implications for Theories of Interval Timing in Humans and Other Animals

The possibility that the gap procedure engages an attentional mechanism was also recently examined in the human literature (Fortin, this volume; Fortin and Masse, 2000). For example, Fortin and Masse (2000) examined whether single-task procedures, like the gap procedure, engage attention-sharing processes in humans. When human participants were extensively trained with both PI and gap trials, after the gap they delayed their response more at longer pregap durations. These data were taken to suggest that participants developed an expectation of the gap, and that the longer the pregap duration, the more this expectation reduced the attentional resources allocated to timing. Therefore, Fortin and Masse's (2000) data suggest that results from the gap procedure can be interpreted in terms of attention sharing between the timer and other cognitive processes (Thomas and Weaver, 1975; Block and Zakay, 1996; Zakay, 1998, 2000). Together with the results from the experiments described in this chapter these findings support the proposal that the attention-sharing model (Block and Zakay, 1996; Thomas and Weaver, 1975; Zakay, 1989, 2000) can be fruitfully applied to the results from the gap procedure in both humans and other animals. In contrast to possible species differences in interval timing strategies (e.g.,

Bateson, 1998; Brodbeck et al., 1998; Roberts et al., 1989), these findings support an integrative approach to the data patterns obtained in interval timing procedures from rodents, birds, and humans.

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