A matching law analysis of the effect of amphetamine on responding reinforced by the opportunity to run.
Lambert (1992) proposed that the pharmacological basis of the rewarding effects of running is a function of a dopamine rather than an opiate mechanism. Specifically, "after moderate running, increased mesolimbic dopaminergic activity provides physiological reinforcement, which sustains maladaptive running in the face of low food consumption" (Lambert, 1992, p. 27). Evidence cited in support of this hypothesis comes from studies of the effects of dopamine agonists and antagonists on running. Dopamine agonists such as amphetamine and cocaine increase running (Evans & Vaccarino, 1986; Glavin, Pare, Vincent, & Tsuda, 1981; Jakubczak & Gomer, 1973; Tainter, 1943) whereas dopamine antagonists such as pimozide and chlorpromazine decrease running (Beninger & Freedman, 1982; Routtenberg, 1968; Routtenberg & Kuznesof, 1967). However, this evidence must be viewed with a degree of skepticism because it fails to distinguish between motor and motivational effects of the drugs. That is, a decrease in running under the influence of a drug may be the result of either a decrease in motivation to run or an impairment of motor behavior.
One procedure that offers the potential to discriminate between motor and motivational changes in reinforced responding due to the effect of a drug is based on Herrnstein's (1970, 1974) matching law (Hamilton, Stellar, & Hart, 1985; Heyman, 1983, 1992; Heyman & Monaghan, 1987, 1990; Heyman, Kinzie, & Seiden, 1986; Heyman & Seiden, 1985). Herrnstein (1970) formulated an elementary matching law equation for the case where there is only a single measured source of reinforcement and a single measured response rate. The relationship between response and reinforcement rates in this case generally takes the form of a negatively accelerated monotonic function that is described by the following equation:
B1 = k R1 / R1 + Re. (1)
In Equation 1, B1 is response rate, R1 is reinforcement rate, and k and Re are estimated parameters. Specifically, k refers to the asymptotic rate of responding (i.e., the maximal response rate) and Re is the rate of reinforcement associated with one half the asymptotic rate of responding. Re describes how quickly response rate rises toward asymptote as reinforcement rate increases and at one half the asymptotic response rate (k/2), the value of Re can be estimated because R1 and Re are equivalent.
The k parameter in Equation 1 has been interpreted as an index of the motor aspects of a reinforced response (Hamilton et al., 1985; Herrnstein, 1974; Heyman, 1983). This interpretation derives from empirical observations that showed that when k changed, but Re remained stable, the experimenter changed some aspect of the response requirement (Heyman & Monaghan, 1987). For example, the value of k changed independent of Re with a change in response topography when the response manipulandum for pigeons was changed from a pecking key to a treadle (McSweeney, 1978) and with a change in response force on the same manipulandum when the force required to make a response was increased (Belke & Heyman, 1994; Heyman & Monaghan, 1987). In addition, Porter and Villanueva (1988) found a relation between response duration and the value of the k parameter. Specifically, as response duration increased, the value of k decreased. Thus, k appears to index motor aspects of performance.
In contrast, the Re parameter has been interpreted as an index of the motivational component of a reinforced response (Heyman & Monaghan, 1987). This interpretation follows from the observation that in studies where Re changed, while k remained stable, experimenters changed either reinforcement magnitude, reinforcement quality, or deprivation level (Heyman & Monaghan, 1987). For example, the value of Re decreased when the body weight of subjects responding for sucrose reinforcement was decreased (Bradshaw, Szabadi, Ruddle, & Pears, 1983) or when the concentration of sucrose reinforcement was increased (Heyman & Monaghan, 1994). In both cases, as motivation to obtain the scheduled reinforcement increased (i.e., with greater deprivation for food and with an increase in the sweetness of the reinforcement), response rate rose more quickly toward asymptote and the value of Re decreased. In contrast, if motivation to obtain the scheduled reinforcement decreased, response rate would rise less quickly toward asymptote and the value of Re would increase. Thus, Re appears to index a motivational aspect of performance.
Belke and Heyman (1994) extended the matching law approach to the study of the relationship between response and reinforcement rates when the opportunity to run was scheduled as the reinforcing consequence for lever pressing. Manipulations of the force required to make a response and access to the wheel demonstrated that the empirical interpretations of the k and Re parameters held when running functioned as a reinforcing consequence. When the force required to make a response was increased by 26 grams, the mean value of k decreased from 61 to 37 responses/minute while the Re remained constant at approximately 93 reinforcers/hour. When access to the wheel was limited by placing the subjects in the locked wheel for 45 minutes prior to a session, the average value of Re decreased from 73 to 51 reinforcers/hour while k remained constant at 57 responses/minute.
Previous research using the matching law procedure to study the effects of drugs on reinforcement efficacy and motor performance has shown that dopamine antagonists such as chlorpromazine and pimozide decrease the efficacy of water (Heyman et al., 1986) and food reinforcement (Heyman, 1983; Willner, Sampson, Phillips, & Muscat, 1990) at low doses. In contrast, dopamine agonists such as amphetamine increase the efficacy of food reinforcement to maintain behavior at low doses (Heyman, 1983, 1992; Heyman & Seiden, 1985). However, this procedure remains to be extended to the investigation of the effects of dopamine agonists on responding maintained by nonappetitive wheel-running reinforcement.
In the present study, subjects were exposed to a series of tandem fixed ratio 1 variable-interval schedules of wheel-running reinforcement and Herrnstein's (1970, 1974) matching law was fit to the obtained response and reinforcement rates. After 60 sessions, subjects were exposed to amphetamine to observe the effects of amphetamine on responding reinforced by the opportunity to run. If amphetamine increases the reinforcing efficacy of running (i.e., motivation to run) then the matching law analysis should reveal that Re decreases while k remains unchanged. This result would be consistent with Lambert's (1992) dopamine hypothesis. Alternatively, if k changes while Re remains unchanged, then the matching law analysis would suggest that amphetamine alters motoric rather than motivational aspects of reinforced responding and this result would not support Lambert's (1992) hypothesis.
Twelve male Wistar rats (Charles River Breeding Laboratories, Que.) were individually housed in polycarbonate cages (20 x 24 x 40 cm) in a holding room on a 12-hr light/dark cycle (lights on 8:00 am). Subjects were maintained at 80% of an initial free-feed body weight with free access to distilled water in the home cage at all times. Under food deprivation conditions, body weights ranged from 288 to 298g.
Subjects were tested in standard activity wheels (3 Wahmann & 5 LaFayette Instruments Model #86041A) located in soundproof shells. Each wheel was 35.5 cm in diameter. A solenoid-operated brake was attached to the base of each wheel. When the solenoid was operated, a rubber tip attached to a metal shaft contacted the wheel and caused the wheel to stop. A retractable lever (Med Associates ENV-112) was mounted at the opening of each wheel so that the lever would protrude into the wheel chamber when extended. A 24-V DC light was mounted on each side of the frame of the wheel to illuminate the interior of the wheel and the area of the lever. Control of experimental events and recording of data were handled by IBM personal computers.
Initially, all rats were given free access to a running wheel for 30 min each day for 10 days. After 10 days, subjects were placed in a standard operant conditioning chamber following the session in the wheel and shaped to press a lever. Each lever press produced 0.1 ml of a 15% sucrose solution. When subjects reliably pressed the lever, the schedule of reinforcement was shifted from a continuous reinforcement schedule through a series of variable-ratio (VR) schedules, including VR 3, VR 6, VR 9, and VR 15. Each schedule was in effect for approximately four sessions.
Throughout the period of lever training, subjects continued to run in wheels daily for a single 30-min session. When four sessions of lever pressing for sucrose solution on the VR 15 schedule were completed, lever pressing for sucrose solution was discontinued. At this time, the retractable lever in the wheel chamber was made operative and the opportunity to run for 60 s was made contingent upon a single lever press. A session consisted of 30 opportunities to run.
Training then proceeded through the following steps. The schedule of reinforcement was successively shifted through the following sequence: fixed ratio (FR) 1 response, VR 3 response, VR 5 response, VR 9 response, and VR 15 response. Subjects remained on each schedule for 3 days before advancing to the next schedule. During this period of training on the series of VR schedules, 8 rats that ran at higher rates and completed all scheduled reinforcements within the shortest duration were chosen to continue with the study. There were two reasons for this selection. First, animals with low response rates and long session durations were not likely to complete all components of a mixed schedule within the drug's half-life. Interpretation of a drug effect using the matching law depends upon all reinforcement schedules being completed while the animal is under the influence of the drug. Note that the half-life for amphetamine varies with the pH of urine and may be as short as 7 hours (McKim, 1991). Second, animals that ran at higher rates typically tended to respond at higher rates (Belke, 1996) and, thus, were more likely to develop response-reinforcement relationships sufficiently well defined so as to permit clear discrimination of motor and motivational effects of the drug treatments (Belke & Heyman, 1994).
Following the 3rd day on the VR 15 schedule, the session was changed to a sequence of four tandem FR 1 variable-interval schedules (VI 5, VI 15, VI 30, VI 60) and the reinforcement period was shifted from 60 s to 30 s. With the change from a response-based (VR) reinforcement requirement to a response-initiated time-based (VI) reinforcement requirement, the operation of the schedule was modified so that a reinforcement interval did not start timing until the first response was made. Thus, after termination of a reinforcement, a new interval was selected, but it did not begin to time out until the first lever press. When the reinforcement interval elapsed, the first lever press caused the lever to retract and the brake to release. The wheel was free to turn for 30 s before the brake was engaged and the lever was extended for the next reinforcement interval. The programmed interreinforcement intervals for the variable interval component of the tandem FR 1 VI schedules approximated an exponential distribution (Fleshler & Hoffman, 1962) and the order of intervals was randomized across sessions.
Within a session, successful completion of 10 reinforcers in each component on a given schedule was followed by a 1-min blackout time during which the lights were turned off and the brake was engaged. When the blackout period expired, the lever extended, the lights were turned on, and the animal was given the opportunity to obtain another 10 reinforcers on a different reinforcement schedule. A session consisted of completion of each of the four schedules of reinforcement for a total of 40 reinforcement periods. Each animal was presented with the same sequence of schedules across all sessions, however, sequences were varied across rats (see Table 1). After each session, animals were weighed and fed a measured amount of food to maintain 80% body weight level.
Animals were given 60 sessions under these conditions to allow for differentiation between response rates on the different schedules, before drug testing commenced. Subjects were then administered d-amphetamine sulfate by intraperitoneal injection 20 min prior to a session at doses of 0.25, 0.5, and 1.0 mg/kg. Each dose was administered three times and the order of dose administration was randomized across rats. Between drug administrations, baseline and saline-vehicle injection sessions occurred.
Dependent measures taken for each session were total lever presses, time spent pressing the lever, postreinforcement latency (latency to press following reinforcement), and wheel revolutions. Local response rates were calculated as the number of lever presses divided by the time spent lever pressing exclusive of latency to respond and expressed as responses/minute. Data obtained from all rats were included in the analysis of drug effects on local response rate, total wheel revolutions, and total postreinforcement latency. A repeated measures analysis of variance (ANOVA) was performed to test for dose effects and Dunnett's t tests were performed to compare means.
Table 1 Data from the Last 5 Sessions Prior to Drug Testing for Each Rat Rat Schedule Order k Re %VAC Revs Resp Lat X09 30 60 15 5 83.0 193.5 94.2* 655 28.1 474 X10 5 30 60 15 31.4 29.4 55.6 610 23.3 1156 X11 5 60 30 15 38.4 33.7 69.1 716 27.1 802 X12 30 5 15 60 53.7 84.4 83.8* 668 28.1 2329 X13 60 15 5 30 42.7 70.9 93.8* 882 23.2 522 X15 60 5 30 15 95.7 71.6 85.3* 820 54.3 908 X18 15 60 5 30 40.2 52.1 64.6 736 24.9 1379 X24 15 30 60 5 48.0 59.9 43.1 522 30.2 1410 Note: The schedule order for each rat is shown followed by the parameters and goodness of fit percentages from Equation 1 fit to the data for each rat averaged over the last five sessions of the baseline condition prior to drug testing. Asterisks denotes rats selected for analysis of drug effects using Equation 1 based on criteria stated in the methods. "% VAC" refers to the percentage of variance in response rates. Also shown are the mean revolutions (Revs), response rate (Resp) (responses/minute), and cumulative latency to respond following the termination of reinforcement (Lat) (seconds) from the last five baseline sessions.
In addition, lever presses, time, and latency to press were recorded for each reinforcement to examine within-session effects on response rates. Wilkinson's (1961) method of estimating the parameters of a hyperbolic function was used to generate k and Re values. A-priori criteria were established for analysis of data from rats that showed systematic differentiation of response rates as a function of reinforcement rates. First, and most importantly, when Equation 1 was fit to response and reinforcement rates averaged over the last five sessions of the baseline condition at least 75% of the variance in response rates had to be accounted for by variance in reinforcement rates (Willner et al., 1990). Second, estimates of k and Re for each session over the last five consecutive sessions could be neither the highest nor the lowest observed under the baseline condition. The rationale for this selection procedure is that if the relationship between response and reinforcement rates is not adequately described by Herrnstein's equation, then the estimated parameters k and Re are unreliable and interpretation of drug effects based on these parameters should not be undertaken. Although all rats met the second criterion, Table 1 shows that only 4 of the 8 rats met the first criterion.
Table 2 Effects of Amphetamine on k and Re Estimates Condition k Re SE k SE Re %VAC Rat X09 Baseline 71 153 9.1 45.7 94 0.00 mg/kg 79 168 12.2 57.3 92 0.25 mg/kg 76 117 9.9 39.0 91 0.50 mg/kg 93 119 8.4 29.2 95 1.00 mg/kg 65 48 4.5 13.7 92 Rat X12 Baseline 58 101 8.7 38.8 84 0.00 mg/kg 57 92 4.4 20.6 96 0.25 mg/kg 55 62 3.1 12.9 96 0.50 mg/kg 37 40 4.2 19.5 79 1.00 mg/kg 43 42 3.5 15.4 89 Rat X13 Baseline 31 59 3.0 19.4 90 0.00 mg/kg 32 44 3.2 18.8 84 0.25 mg/kg 31 22 1.7 8.0 85 0.50 mg/kg 31 24 1.8 8.7 84 1.00 mg/kg 27 11 0.9 4.2 79 Rat X15 Baseline 101 79 8.3 20.4 95 0.00 mg/kg 96 62 9.3 21.4 89 0.25 mg/kg 88 54 9.0 19.7 85 0.50 mg/kg 85 55 9.1 20.9 85 Note. Parameters and goodness of fit percentages from Equation 1 fit to the data for the rats that met the inclusion criteria. Conditions were baseline, 0.0 mg/kg, 0.25 mg/kg, 0.50 mg/kg, and 1.0 mg/kg doses of amphetamine. "%VAC" refers to the percentage of variance in response rates accounted for by variance in reinforcement rates. Standard errors for the estimates of k and Re are given.
The effect of amphetamine on responding within sessions was evaluated through a matching law analysis of the relationship between response and reinforcement rates. This analysis was conducted on data from all animals; however, interpretation of the effects of amphetamine was limited to only those animals that met the previously outlined criteria. Estimates of k, Re, standard errors, and variance accounted for each condition for these subjects are provided in Table 2 and the results for the remaining subjects are tabled in the appendix.
Figure 1 shows the effect of amphetamine by dose on the relationship between response and reinforcement rates for each subject. Figure 2 shows mean percent change in estimates of k and Re relative to baseline values as a function of amphetamine dose. On average, k increased by 2% for the 0.0 mg/kg dose (i.e., saline-vehicle) and decreased by 2.8, 5.3, and 28.6% for the 0.25, 0.5, and 1.0 mg/kg doses, respectively. A repeated measures ANOVA revealed no significant effect of dose on k, F(4, 12) = 2.91, p [greater than] .05. Post hoc Dunnett's t-test comparisons revealed that the decrease in k produced by the 1.0 mg/kg dose approached significance, [t.sub.d](12) = 2.78, p [less than] .10.
In contrast, Re was decreased by 12.0, 39.1, 43.1, and 80.6% relative to baseline for the 0.0, 0.25, 0.5, and 1.0 mg/kg doses, respectively. A repeated measures ANOVA revealed a significant effect of dose on Re, F(4, 12) = 16.69, p [less than] .001. Post-hoc Dunnett's t-test comparisons with baseline revealed significant changes for the 0.25 mg/kg dose, [t.sub.d](12) = 3.60, p [less than] .05; the 0.5 mg/kg dose, [t.sub.d](12) = 3.97, p [less than] .01; and the 1.0 mg/kg dose, [t.sub.d](12) = 7.42, p [less than] .01.
With respect to the effect of amphetamine on local response rate, cumulative latency to respond, and total revolutions over the entire session, no significant effects were observed. For this analysis, the data from all 8 rats were used. Relative to baseline, local response rates increased on average 1.6, 6.6, and 15.5% for the 0.0, 0.25, and 0.5 mg/kg doses, but decreased by 3.0% for the 1.0 mg/kg doses. None of these changes attained significance, F(4, 28) = 1.48, p [greater than] .10. Cumulative latency to respond increased on average by 7.7, 8.1, 11.9, and 18.8% for the 0.0, 0.25, 0.5, and 1.0 mg/kg doses, respectively. As with response rates, there was no significant drug effect, F(4, 28) = 0.67, p [greater than] .10. Finally, total revolutions increased by 1.3% for the 0.0 mg/kg dose, but decreased by 6.3, 1.7, and 8.1% for the 0.25, 0.5, and 1.0 mg/kg doses, respectively. Analysis revealed a drug effect, F(4, 28) = 3.24, p [less than] .05; however, no dose produced a significant effect relative to baseline. Note that restricting the analysis of local response rate, cumulative latency, and total revolutions to only the data from the 4 rats that met the criteria for the matching law analysis also revealed no significant drug effects; F(4, 12) = 1.02, p [greater than] .10, F(4, 12) = 0.16, p [greater than] .10, F(4, 12) = 0.90. p [greater than] .10, respectively.
Finally, mean session durations averaged across all animals for the baseline, 0.0 mg/kg, 0.25 mg/kg, 0.50 mg/kg, and 1.0 mg/kg conditions were 4238, 4397, 4478, 4495, and 4838 s, respectively. Session durations in all conditions were within the half-life of amphetamine.
In the present study, the effect of amphetamine on responding reinforced by the opportunity to run for a brief period of time was investigated using Herrnstein's (1970, 1974) matching law equation. Changes in the relationship between response and reinforcement rates under the influence of amphetamine were consistent with the interpretation that amphetamine increased the reinforcing efficacy of running. Specifically, amphetamine decreased Re while the value of k remained relatively unchanged. The empirical basis for this interpretation comes from studies that have shown that decreases in Re independent of changes in k occur when reinforcement quality, reinforcement magnitude, and deprivation level were manipulated (Bradshaw, Ruddle, & Szabadi, 1981; Bradshaw, Szabadi, & Bevan, 1978; Bradshaw et al., 1983; Conrad & Sidman, 1956; Guttman, 1954; Heyman & Monaghan, 1987, 1994, deVilliers & Herrnstein, 1976, analyzed results for studies prior to 1976). Furthermore, the results were consistent with previous studies using a matching law analysis that have shown that dopamine agonists (i.e., amphetamine, methylphenidate) increase the reinforcing efficacy of the experimentally arranged reinforcement (i.e., milk, sucrose solution) (Heyman, 1983, 1992; Heyman & Seiden, 1985).
Paradoxically, although the reinforcing efficacy of running, as indexed through the relationship between response and reinforcement rates, increased, running did not increase. On the contrary, revolutions decreased across the dose range that increased the reinforcing value of running, though not significantly so. However, this paradox may be more apparent than real. Previous research has shown that as the duration of the opportunity to run decreases, rate of running increases toward an asymptotic level (Belke, in press). Thus, the brief duration used as reinforcement in the present study to ensure that session duration fell within the drug's half-life probably induced near asymptotic rates of running. Consequently, with running near a behavioral ceiling, it is unlikely that a psychomotor stimulant such as amphetamine would increase running.
Finally, the results lend tentative support to Lambert's (1992) hypothesis that the pharmacological basis for the reinforcing value of running is dopaminergic. The present study represents an advance over previous studies that investigated the effects of drugs, such as amphetamine, directly on running. Increases or decreases in running under these conditions could represent either a motivational or a motor effect. In the present study, operant responding maintained by the opportunity to run represented an index of the reinforcing efficacy of running and changes in the relationship between response and reinforcement rates provided a means to distinguish changes in the motor and motivational components of a reinforced response. Further substantiation that the effect is motivational would come with future research negating the possibility that the observed changes were caused by either central or peripheral adrenergic effects of amphetamine.
The finding that the pharmacological basis of the rewarding properties of running may involve dopamine is also consistent with previous research showing that dopamine plays an important role in preparatory behavior (Blackburn, Phillips, & Fibiger, 1987; Blackburn, Phillips, Jakubovic, & Fibiger, 1989). Ethologists distinguish between preparatory and consummatory behavior. With respect to food, consummatory behaviors occur when animal has made contact with a food item and result in the ingestion of the food. Examples of consummatory behaviors are biting, chewing, and swallowing. In contrast, preparatory behaviors refer to "appetitive acts that typically lead to, or make possible, consummatory behavior" (Blackburn et al., 1987, p. 352) that are elicited by biologically significant events known as "incentive stimuli." Examples of preparatory behaviors are foraging and hoarding. It is possible that the pharmacological basis of the reinforcing value of running is related to the role of activity in foraging for food, as such, it would be an example of a preparatory behavior. Although it is important to note that in the context of the present study, there was no explicit incentive stimulus (i.e., food item) that would elicit running as a preparatory behavior. However, it may be the case that interoceptive stimulation associated with food deprivation may serve this function (Davidson, 1993).
In sum, although the widely known opiate hypothesis for "runner's high" would imply that the reinforcing properties of running are a function of endogenous opiates, results from the present study suggest otherwise. Changes in the response-reinforcement rate functions under the influence of amphetamine in the present study suggest that amphetamine enhanced the reinforcing efficacy of the opportunity to run. Therefore, the results from the present study, although not negating the opiate hypothesis, lend support to the alternative dopamine hypothesis. Further support for the dopamine hypothesis may come with future investigation of the effects of selective dopamine antagonists on responding reinforced by the opportunity to run.
This report is based on an undergraduate thesis submitted by Jason Neubauer in partial fulfillment of a BA degree at Mount Allison University, Sackville, Canada that extends an initial investigation from the doctoral dissertation of Terry Belke. This research was supported by Grant OGP0170022 from the Natural Sciences and Engineering Research Council of Canada to Terry W. Belke. Correspondence regarding this article should be sent to Terry W. Belke, Department of Psychology, Mount Allison University, Sackville, New Brunswick, Canada, E0A 3C0 or via E-mail to TBELKE@MTA.CA.
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Parameters and goodness of fit percentages from Equation 1 fit to the data for the rats that did not meet the inclusion criteria. Conditions were baseline, 0.0 mg/kg, 0.25 mg/kg, 0.50 mg/kg, and 1.0 mg/kg doses of amphetamine. Standard errors for the estimates of k and Re are given. Note that estimates of variance accounted for (%VAC) are low while standard errors for the estimates of Re tend to be larger than the estimates. With the exception of the 0.50 mg/kg condition, the data for Rat X11 is adequately described; however, inclusion of data for this rat would not alter the findings of the study.
Rat X10 Condition k Re SE k SE Re % VAC Baseline 25 11 3.0 13.9 23 0.00 mg/kg 21 6 5.7 32.3 -26 0.25 mg/kg 24 25 4.9 26.9 22 0.50 mg/kg 29 19 1.6 7.5 82 1.00 mg/kg 20 44 5.7 39.2 21 Rat X11 Condition k Re SE k SE Re % VAC Baseline 38 37 3.1 14.1 86 0.00 mg/kg 35 30 4.4 20.2 68 0.25 mg/kg 39 32 3.4 13.9 82 0.50 mg/kg 28 7 3.5 14.0 7 1.00 mg/kg 35 10 0.4 1.5 97 Rat X18 Condition k Re SE k SE Re % VAC Baseline 41 55 12.5 61.3 29 0.00 mg/kg 33 32 7.9 37.7 29 0.25 mg/kg 29 25 7.8 38.1 10 0.50 mg/kg 36 26 3.0 12.8 77 1.00 mg/kg 29 34 9.8 41.8 -10 Rat X24 Condition k Re SE k SE Re % VAC Baseline 46 93 14.9 73.6 34 0.00 mg/kg 51 114 14.6 72.0 48 0.25 mg/kg 36 66 5.5 33.0 77 0.50 mg/kg 36 20 4.6 18.3 39 1.00 mg/kg 13 -6 2.3 14.2 -4
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|Author:||Belke, Terry W.; Neubauer, Jason|
|Publication:||The Psychological Record|
|Date:||Jun 22, 1997|
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