The effect of water deprivation on shock-escape impairment after exposure to inescapable shock.
One investigation of the contribution of the motivational deficit to the shock-escape impairment seen in the traditional shuttlebox test was provided by Jackson, Maier, and Rapaport (1978), who exposed rats, pretrained with inescapable shock, to three different levels of test shock intensity ranging from 0.6 mA to 1.0 mA. The typical interference effect seen at 0.6 mA was eliminated with shocks of higher intensity. In addition, in an escape extinction test, the number of trials on which a rat made two or more shuttle crossings was significantly greater with 1.0 mA shock than with 0.6 mA shock. One way to view this is as a manipulation of the aversive drive level present during the shuttle test. The results, therefore, suggest that an increase in drive, because of a potential attendant increase in activity, can overcome the effects of the motivational deficit revealed by impaired escape performance in the shuttlebox. In other words, if the probability of a response can be increased, the effects of the associative deficit can be overcome.
Recently, Balleine and Job (1991) have reported evidence suggesting that manipulations of activity, or more precisely inactivity, during training can also affect performance during a shuttle box escape test. Using rats, their data demonstrated that, if a long inactivity response (ascending scale, range 2 s to 18 s) was required to terminate shock, the subsequent two crossings (FR2) escape performance of escapable shock animals was significantly impaired relative to either a yoked inescapable shock group, which received the same shock density, or an escapable shock group which could terminate shock following a short, 2-second, inactive response. Further, the amount of inactivity during shock was the best predictor of shuttle escape performance irrespective of whether the rat had been exposed to escapable or inescapable shock. Although Maier (1970), using dogs, demonstrated that a 2-s inactive response did not impair escape performance compared to a yoked inescapable shocked group, attempts to replicate these findings with rats (e.g., Anderson, Crowell, Cunningham, & Lupo, 1979) produced results that were similar in form to those of Balleine and Job (1991). These data are also consistent with those of Glazer and Weiss (1976a, 1976b), who offered the "learned inactivity" hypothesis, which suggested that, whereas shock initially elicits activity, the level of activity decreases and subjects become more immobile over shocks of longer duration (e.g., 5 s or more). According to this view, immobility is adventitiously reinforced by shock offset and produces a competing response which transfers to the escape task. Apparently, then, manipulations of the level of activity of a rat during either the training or test phases of the traditional learned helplessness procedure can affect performance during the FR2 shuttle escape task.
The interaction of appetitive drive manipulations with aversive drives has been investigated using operant escape or avoidance procedures. Reviews of this literature suggest that there is little effect of an irrelevant appetitive drive manipulation on response-contingent shock motivated behavior (see Bolles, 1975, and Mackintosh, 1974, for reviews). Although the influence of appetitive drive manipulations has been studied with respect to escape and avoidance behavior, no similar systematic investigation has been made of the interaction of appetitive drives with the effects of inescapable shock. Missanin and Campbell (1969) specifically tested rats' responsiveness to inescapable shock under both food and water deprivation conditions. Their findings suggest that, in the presence of inescapable shock, at least in the intensity range that is typically used in tests for learned helplessness, water deprived rats showed some increase in their level of activity as measured by the number of shuttle crossings when compared to nondeprived controls.
The present experiments were designed to assess the interaction of water deprivation with the effects of inescapable shock exposure, both during exposure to inescapable shock and on a subsequent test for shuttle escape acquisition. Water deprivation was chosen as the appetitive drive, because the results of Missanin and Campbell (1969) indicate that water deprivation was more effective than food deprivation in increasing activity during exposure to inescapable shock. In addition, because some evidence suggests that shocks of longer duration (e.g., 5 s or more) may differentially produce competing behavior that can interfere with the subsequent acquisition of escape responding (Glazer & Weiss, 1976a, 1976b), a procedure was used to ensure the administration of relatively long duration inescapable shocks. In this case, any increase in activity produced by water deprivation may work to reduce the passivity engendered by shocks of longer duration.
For the first experiment in this series, animals were deprived during both training and test conditions. Given the unknown interaction between appetitive and aversive drive in the case of inescapable shock, it was considered important to maintain the appetitive drive during both exposure to inescapable shock and during the shuttle box escape test 24 hours later.
Thirty-six male Holtzman rats, weighing 300-400 g at the start of the experiment, served as subjects. They were individually housed and maintained on ad lib food throughout the experiment.
The apparatus consisted of two distinct and separate units. Training was administered in six operant chambers (Lehigh Valley Electronics Model 11414), consisting of Plexiglas sidewalls and ceiling, stainless steel front and rear walls, and a grid floor. The internal dimensions were 30.2 cm long, 24.0 cm wide, and 36.8 cm high. A stainless steel lever (LVE Model 1352) requiring a force of approximately 0.1 N to depress and measuring 2.7 cm wide and 0.9 cm in thickness, protruded 2.15 cm through the front wall. The lever center was located 3.0 cm above the grid floor, 3.5 cm from the rightmost sidewall. Stainless steel grid bars, 0.5 cm in diameter, mounted perpendicular to the side walls and spaced 1.8 cm apart (center to center), provided the shock delivery surface. Scrambled constant-current AC shocks, 1.0 mA in intensity, measured at the grids, were delivered by a Coulbourn Instruments Model E13-16 solid state shocker/distributor. Each chamber was enclosed in a sound-attenuating shell.
Escape testing was conducted in a 19.0-cm wide x 22.5-cm high x 46.0-cm long shuttle box, consisting of stainless steel end walls joined by Plexiglas sidewalls and ceiling, housed in a sound-attenuating shell. The shuttle box was divided into two halves by a stainless steel partition which had a 6- x 7-cm rounded archway cut out of it. Each of the shuttle box chambers had 20 stainless steel grids, 0.5 cm in diameter and 0.95 cm from center to center, serving as the shock delivery surface. Each half of the shuttle box was in contact with a microswitch that could terminate shock when an animal crossed from one compartment to the other (FR1) or when it crossed and recrossed (FR 2). A 0.6-mA scrambled constant-current AC shock was delivered from a Coulbourn Instruments E13-16 shock generator to the grid floor on both sides of the shuttle box.
Programming was accomplished using Medstate Notation Language (Thomas Tatham, (c) 1991) run on an IBM compatible computer, interfaced to the experimental chambers via a Med Associates interface. This equipment was located in a room adjacent to the experimental chambers.
Water deprivation. Subjects were randomly assigned to one of three groups. Group ISWD, inescapable shock water deprived, and Group NSWD, no-shock water deprived, were deprived of water beginning 72 hours before exposure to inescapable shock or shock context. On the 2 days preceding training, both groups were given access to 5 min of water daily. On the training day they received 5-min access to water following the specific training procedure. On the test day, there was no access to water prior to the shuttle box test. Group ISW, inescapable shock watered, was maintained on ad lib water for the entire experiment.
Training. ISWD and ISW rats were exposed to 100 unsignaled 1.0-mA shocks. The mean intershock interval was 60 s, with a range of 20120 s. The mean shock duration was 6.7 s with a range from 2-30 s. The order and duration of each shock was derived from actual data produced by rats exposed to a lever press escape contingency that had been run in other experiments in our laboratory. In those experiments, these shocks were terminated by a single lever press only after 2 s of exposure and terminated automatically if no response occurred after 30 s. These latencies were inserted into the computer program controlling each session, so that each pair of ISWD and ISW animals was exposed to a unique distribution of shock as defined by order and duration. This procedure was utilized, as opposed to a fixed duration shock, so as to be more comparable with past research in our laboratory which utilized escapably shocked and yoked inescapably shocked animals. NSWD animals were placed in the training chambers for the duration of the training session, but no shock was delivered.
Testing. Twenty-four hours after the training session, the animals in each group were given five unsignaled FR 1 escape trials in a shuttle box, during which crossing from one side to the other terminated shock. Immediately following these FR 1 trials, each animal received 30 unsignaled FR 2 escape trials, during which two crossings (back and forth) were required to terminate shock. Shock intensity was 0.6 mA. If an animal failed to perform the required response, shock terminated automatically after 60 s. The intertrial interval was 60 s, with a range from 20-120 s.
Results and Discussion
Three measures were used to evaluate shuttle box escape performance: FR1 latency, FR2 latency, and number of failures. Group ISWD and NSWD were equally proficient at escaping on the five FR1 trials. Although Group ISW rats were slower to escape in FR1, this difference was found to be nonsignificant by a one-way ANOVA, F(2, 33) = 1.509, p [greater than] .23. Figure 1 shows FR2 escape latencies in 5-trial blocks. Groups ISWD and NSWD were equally proficient in escaping across trials and Group ISW was slower. A repeated measures ANOVA (treatment x trials) yielded a significant main effect for treatment, F(2, 33) = 5.308, p [less than] .02. There was no significant effect for trials, F(5, 165) = 1.220, p [greater than] .3 or treatment x trials interaction, F(10, 165) = 0.612, p [greater than] .8. Tukey post hoc comparison tests ([Alpha] = .05) demonstrated that there was no difference between Groups ISWD and NSWD, but that both of these groups had significantly shorter latencies than Group ISW. Similarly, a one-way ANOVA of failures to escape was significant, F(2, 33) = 7.177, p [less than] .003.
The results of this experiment suggest that water deprivation can interact with an aversive drive established through exposure to inescapable shock, perhaps through an increase in activity. The effect is to ameliorate the escape impairment normally seen in a shuttlebox escape task 24 hours later. The mean FR2 latency for Group ISWD was comparable to that for Group NSWD, suggesting that water deprivation could summate with the aversive drive maintained by exposure to shock, so that escape impairment is eliminated.
Although the results of Experiment 1 demonstrate that water deprivation can ameliorate the escape impairment normally seen following exposure to inescapable shock, it does not identify whether deprivation during the training or test phase alone is sufficient to overcome the escape impairment normally seen. Therefore, Experiment 2 was conducted to explore the possibility that rats who were maintained on ad lib water through training, but deprived for 24 hours prior to test, would show a reduction in escape impairment.
Thirty-six male Holtzman rats, weighing 300-400 grams at the start of the experiment, served as subjects. They were individually housed and maintained on ad lib food throughout the experiment.
The apparatus was the same as used in Experiment 1.
Water deprivation. Subjects were randomly assigned to one of three groups. Group ISWD, inescapable shock water deprived, and NSWD, no-shock water deprived, were deprived of water beginning immediately following exposure to inescapable shock or shock context. On the test day, there was no access to water prior to the shuttle box test. Group ISW, inescapable shock watered, was maintained on ad lib water for the entire experiment.
Training and test. Training and test procedures were identical to those employed in Experiment 1.
Results and Discussion
A one-way ANOVA showed that there were no significant differences in FR1 latencies for any of the groups, F(2, 33) = 1.204, p [greater than] .3. Figure 2 shows FR2 escape latencies in 5-trial blocks. Groups ISWD and NSWD were equally proficient in escaping across trials and Group ISW was slower. A repeated measures ANOVA (treatment x trials) yielded a significant main effect for treatment, F(2, 33) = 7.453, p [less than] .003. Although there was a significant effect for trials, F(5, 165) = 3.528, p [less than] .006, there was no significant treatment x trials interaction, F(10, 165) = 0.612, p [greater than] .8. Tukey post hoc tests ([Alpha] = .05) showed that both Groups ISWD and NSWD had significantly shorter FR2 latencies than Group ISW while not differing significantly from each other. Similarly, a one-way ANOVA on the number of failures to escape was significant, F(2, 33) = 5. 177, p [less than] .01.
The results of Experiment 2 are similar to those of Experiment 1. This could suggest that the results of Experiment 1 were caused by an increase in appetitive drive produced by water deprivation during the shuttlebox escape test. These results, then, are similar to those of Jackson et al. (1978), who eliminated the escape impairment by increasing aversive drive during the shuttle box escape test.
The results of Experiment 2 suggest that water deprivation during test, like an increase in test shock intensity, is sufficient to disrupt the escape impairment typically seen in the FR2 shuttle escape task following exposure to inescapable shock. It has been demonstrated that the induction of inactivity during exposure to shock, even when the shock is escapable, impairs escape performance 24 hours later in the shuttlebox (Balleine & Job, 1991) This experiment attempted to determine whether water deprivation during the training session in which animals were exposed to inescapable shock will alleviate later shock-escape impairment.
Forty-eight male Holtzman rats, weighing 300-400 grams at the start of the experiment, served as subjects. They were individually housed and maintained on ad lib food throughout the experiment.
The apparatus was the same as used in Experiment 1.
Water deprivation. A 2 x 2 factorial design was used. Subjects were randomly assigned to one of four groups. Group ISWD, inescapable shock water deprived, and NSWD, no-shock water deprived, were deprived of water beginning 36 hours prior to exposure to inescapable shock or shock context, with 5-minute access to water per day. They were returned to ad lib water immediately following exposure to inescapable shock and were maintained on ad lib water for the balance of the experiment. Group ISW, inescapable shock watered and NSW, no-shock watered, were maintained on ad lib water for the entire experiment. Although nondeprived, no-shock animals run in many previous experiments showed no shock-escape impairment, the last group was added to determine whether water deprivation affected performance of such animals.
Training and test. Training and test procedures were identical to those employed in Experiment 1.
Results and Discussion
A two-way ANOVA showed that there were no significant differences in FR1 latencies. Figure 3 shows FR2 escape latencies in 5-trial blocks. Groups ISWD, NSWD, and NSW were equally proficient in escaping across trials and Group ISW was slower. A two-way repeated measures ANOVA yielded a significant main effect for both shock condition, F(1, 42) = 7.111, p [less than] .02, deprivation condition, F(1, 42) = 4.232, p [less than] .02, as well as a shock by deprivation interaction, F(1, 42) = 11.587, p [less than] .002. Although there was a significant effect for trials, F(5, 210) = 3.513, p [less than] .006, there were no significant interactions. Tukey post hoc comparison tests ([Alpha] = .05) show that Groups ISWD, NSWD, and NSW differ significantly from Group ISW, but were not significantly different from each other. A two-way ANOVA of escape failures was significant only for the shock-deprivation interaction, F(1, 44) = 4.619, p [less than] .04, but fell short of significance for the shock condition.
Although the instrumentation for this experiment did not include a precise measure of shock elicited activity, lever press activity during shock was recorded, even though these responses had no contingent relationship to shock termination. Given that shock onset elicits bursts of activity, they do, however, serve as a gross indicator of general activity in response to shock presentations. Because the rats in Experiments 1 and 3 were similarly treated with respect to water availability, the shock-elicited lever press data were combined across experiments for Groups ISWD and ISW. Figure 4 shows the lever press activity. A t test of this activity showed that the water deprived animals made significantly more shock-elicited lever presses than those animals with ad lib access to water, t(23) = 2.590, p [less than] .02.
Despite the fact that lever presses represent a limited and indirect measure of shock-elicited activity, they presumably do reflect a greater level of overall activity in the presence of inescapable shock. This could be important given the longer mean exposure to inescapable shock utilized in this experiment. As argued by Glazer and Weiss (1976a, 1976b), the inactivity that emerges with shocks of longer duration may be adventitiously reinforced by shock offset. This can then transfer to the shuttle escape task. This is also consistent with the results of Balleine and Job (1991).
One interpretation that these data suggest is that water deprivation may increase motivation or drive levels with an attendant increase in activity during inescapable shock exposure, at least partially counteracting the passivity normally observed. In turn, such increased activity may transfer 24 hours later to the shuttlebox test, ameliorating or eliminating shock escape impairment. However, this interpretation is based upon the assumption that reintroduction of ad lib water 24 hours before the shuttlebox test equalized drive conditions for nondeprived and previously deprived animals. There is some experimental evidence suggesting that exposure to inescapable shock reduces normal appetitive behavior, although this work examined nondeprived animals (Desan, Silbert, & Maier, 1988; Maier, Silbert, Woodmansee, & Desan, 1990).
This experiment was performed to determine whether animals that were water deprived prior to inescapable shock exposure and given ad lib access to water during the 24 hours post-shock consume more water than nondeprived controls and show evidence of compensation by drinking more water than during a baseline period prior to deprivation. Evidence for such compensation would indicate that exposure to inescapable shock does not suppress appetitive behavior in deprived rats and would suggest that drive conditions at the time of the shuttlebox test in Experiment 3a were the same for deprived and nondeprived animals.
The subjects were 24 male Holtzman rats, 500-600 g at the start of the experiment. They were given ad lib access to food.
Inescapable shock exposure occurred in the operant chambers described in Experiment 1. No shuttlebox test was run.
A matched pairs design was used. Animals were ranked for baseline water consumption, based upon the mean consumption for the 3 days prior to the start of deprivation for the deprived group. Animals within pairs were assigned at random to the deprived (ISWD) and nondeprived (ISW) groups. Water deprivation for Group ISWD was the same as for that group in Experiment 3a. Group ISW had ad lib access to water. Inescapable shock exposure was that described in Experiment 3a. Members of a pair were run together, so that they received identical shock exposure. Water consumption was measured for the 24 hours post-shock.
Results and Discussion
The water consumption data were analyzed by paired-sample t tests. Water consumption was reliably greater for Group ISWD than for Group ISW, t(11) = 6.721, p [less than] .001. On the average, deprived animals consumed 22.75 ml more water than nondeprived animals, and, in 11 out of 12 pairs, the deprived animal drank more than the nondeprived animal. Furthermore, deprived animals consumed more water (M: 25.98 ml) during the 24 hours post-shock than during baseline, t(11) = 7.447, p [less than] .001, whereas the difference for nondeprived animals (M = -2.3 ml) was not reliable (t [less than] 1.0).
These data suggest that under the conditions utilized in this experiment, exposure to inescapable shock does not suppress water consumption in deprived animals. However, the small decrease in nondeprived animals is in the same direction as that found by Desan et al. (1988) and Maier et al. (1990). Further, the highly significant increase in water consumption, relative to baseline in deprived rats, suggests that these animals compensated for the earlier deprivation manipulation. Accordingly, the elimination of shock-escape impairment in the shuttlebox for deprived animals in Experiment 3a is not easily attributed to a difference in drive relative to nondeprived animals during the test. This suggests that water deprivation prior to inescapable shock exposure, perhaps through an increase in activity at least partially counteracting the passivity produced by the shock, may lead to an increase in activity during the test. Such an increase, like that resulting from an increase in test shock intensity, leads to more FR 2 crossings with attendant negative reinforcement from shock termination. Thus, variables affecting either appetitive or aversive drive during inescapable shock exposure or the shuttlebox test can determine shock-escape performance during the test, probably through an attendant effect on activity.
The present research was designed to test the contribution of the motivational deficit to the shock-escape impairment normally seen following exposure to inescapable shock. It also evaluated whether the manipulation of an appetitive drive rather than an aversive drive could affect behavior motivated by exposure to inescapable shock. The results of these experiments suggest that water deprivation is capable of ameliorating this escape impairment.
Experiments 1 and 2 can be interpreted parsimoniously to demonstrate that water deprivation during the shuttlebox test, like increased shock intensity during the test, is capable of eliminating the shock-escape impairment typically observed following exposure to inescapable shock. In contrast, the results of Experiment 3a suggest that water deprivation in effect only during inescapable shock exposure is sufficient to eliminate shock-escape impairment during a shuttlebox test 24 hours later. The results of these experiments are consistent with those of Jackson et al. (1978). These authors found no differences in FR2 escape latency among restraint control groups tested at 0.6, 0.8, or 1.0 mA. However, in animals preexposed to inescapable shock, those animals tested at 0.6 mA had significantly longer escape latencies than those tested at both 0.8 and 1.0 mA, with no impairment evident with the 1.0 mA test shock. Similarly, the findings of Experiment 3a of this series showed that an increase in appetitive drive during training improved escape performance only for rats that were exposed to inescapable shock. Nonshocked controls showed no difference in escape performance whether deprived or not.
The basis for this effect is assumed to be increased activity engendered by water deprivation either during inescapable shock exposure, which then transfers to the shuttlebox test, or directly during escape performance in the shuttlebox test. The limited data for shock-induced lever pressing provides some support for this interpretation. Although the results of research on the effects of water deprivation upon general locomotor activity are mixed (e.g., Campbell, 1960; Finger & Reid, 1952; Hall, 1955), it is reasonable to assume that it may increase activity from the depressed level produced by exposure to inescapable shock (cf. Missanin & Campbell, 1969).
Our findings also appear to be inconsistent with earlier data suggesting that appetitive drive operations have no significant effect on aversively motivated behavior. For example, Mackintosh (1974) reports that there is little evidence to indicate that an increase in appetitive drive will facilitate aversively motivated behavior. However, most of the experimental work done in this area has examined the effects of food or water deprivation on the acquisition of escape or avoidance behavior in the absence of any prior exposure to aversive events. Accordingly, activity level was not depressed, and responding was maintained by the negative reinforcement from shock termination or avoidance. Therefore, it is not surprising that an appetitive drive might have little or no effect upon performance. On balance, there are almost no data bearing upon the effect of an appetitive drive operation on performance of animals exposed to uncontrollable aversive events. Missanin and Campbell (1969) demonstrated an increased number of shuttlebox crossings within the range of deprivation and shock intensity utilized in the present experiments. Additional evidence that an appetitive drive can summate with an aversive drive is provided by Dinsmoor (1958), who investigated the effect of the interaction of prior inescapable shock exposure and food deprivation upon the acquisition of an escape response. Although Dinsmoor did not make any direct comparisons between deprived and nondeprived rats, it is clear from a review of his data that deprived inescapably shocked rats made more escape responses than nondeprived inescapably shocked rats, although fewer than nonshocked control rats. These findings are consistent with the observation in Experiment 3a that the escape performance of deprived inescapably shocked rats was significantly better than that of nondeprived inescapably shocked rats, and, in this case, not reliably different from that of no-shock animals whether deprived or not. The results of both Experiment 3a and those of Dinsmoor may be caused by an increase in activity produced by an appetitive drive, made apparent only when activity has otherwise been depressed by exposure to inescapable shock.
The results from Experiment 3b are consistent with findings showing that exposure to inescapable shock suppresses water intake in nondeprived rats (Desan et al., 1988; Maier et al., 1990). Nondeprived inescapably shocked rats in Experiment 3b of this series showed a slight suppression in water consumption (-2.3 ml) when compared to baseline. However, deprived inescapably shocked rats in that experiment significantly increased their water consumption over baseline levels (+25.98 ml), suggesting that water deprivation more than counteracts the suppressive effect of inescapable shock preexposure. Because it is impossible to provide a precise measure determining the comparability of drive levels between the two groups, the significant increase in water consumption over baseline for the deprived rats, when coupled with the slight decrease for the nondeprived rats, suggests that the two groups were comparable at the time of the shuttlebox test. It should be noted that, despite suppression in water consumption by nondeprived rats previously exposed to inescapable shock, perhaps implying some water deprivation, their escape performance in the shuttlebox did not improve. Accordingly, minor differences in drive level at the time of the shuttlebox test between the deprived and nondeprived inescapably shocked groups should have had little or no effect upon escape acquisition.
The results from Experiment 3a are of particular interest. In both Experiments 1 and 2, water deprivation may have had its effect directly on shuttle escape performance. However, in Experiment 3a rats were water deprived only during inescapable shock exposure. As demonstrated by Balleine and Job (1991), learning an FR2 escape response can be problematic for rats, even rats exposed to escapable shock, if the earlier escape response required passivity. It is assumed that this passivity then transfers to the shuttlebox and interferes with learning an FR2 response. In Experiment 3a, it is assumed that water deprivation increases activity elicited by the onset of shock. This may be especially critical because of the longer mean duration of shock used in this experiment. As argued by Glazer and Weiss (1976a, 1976b), the inactivity that emerges towards the end of long duration inescapable shock may become adventitiously conditioned to shock offset. Just as in the case of Balleine and Job (1991), this response could then transfer to the shuttlebox and interfere with learning an FR2 response.
Exposure to inescapable shock, in the absence of any other motivational operation, has been shown to decrease the expression of many behaviors (Desan et al., 1988; Maier et al., 1990; Woodmansee, Silbert, & Maier, 1993). This general effect can be broadly described as due, at least in part, to a general reduction in activity. This reduced probability of response is characteristic of the motivational deficit produced by exposure to inescapable shock.
One mechanism advanced to account for this general reduction in activity is the depletion in norepinephrine produced by exposure to inescapable shock (Weiss, Glazer, & Pohorecky, 1975). Those findings suggest that any operation that promotes an increase in norepinephrine may be able to overcome the motor suppressive effects of prior exposure to inescapable shock. Water deprivation has been shown to increase norepinephrine metabolism in rats (Klemfus & Seiden, 1985; Luttinger & Seiden, 1981). One possible explanation for the results of the current experiments is that water deprivation increased levels of norepinephrine above the depressed levels normally seen following exposure to inescapable shock. This putative increase in norepinephrine may then underlie the increase in activity assumed to be responsible for overcoming the shock-escape impairment by the water-deprived rats in these experiments.
A recent attempt to assess the effect of drugs that increase activity on shuttlebox escape performance following inescapable tail shock has produced some support for the view that increasing activity ameliorates the shock-escape impairment typically seen (Minor, Chang, & Winslow, 1994). In these tests, caffeine administered prior to the shuttlebox test reversed the escape deficits normally seen in rats exposed to inescapable shock. Caffeine administered prior to inescapable shock exposure had no effect, but rats in these experiments were in restraint tubes, where the effects of stimulant drugs on activity would be negligible. interestingly, amphetamine given before the shuttle box test had no effect on escape deficits. A potential explanation is that amphetamine produces increases in activity that generally emerge as stereotypic behaviors. Engaging in these behaviors may then actually interfere with the learning of an escape response.
Water deprivation manipulations have also been shown to increase the pain threshold in mice as assessed by a hot plate test (Konecka, Sroczynska, & Przewlocki, 1985). Because naltrexone abolished this effect, it is assumed that water deprivation recruits an opioid response. However, if this were the case in the present series of experiments, the opioid response would reduce the perceived intensity of shock. This, it could be argued, would produce results similar to those demonstrated by Jackson et al. (1978), that is greater shock-escape impairment at lower test shock intensities.
In summary, the present research indicates that water deprivation, either at the time of inescapable shock exposure, or prior to a shuttlebox test for shock escape acquisition 24 hours later, can ameliorate or eliminate the escape impairment that typically follows inescapable shock exposure. These results are consistent with the findings of both Balleine and Job (1991), who demonstrated that manipulating activity levels during inescapable shock exposure influenced performance during a subsequent shuttlebox test, and Jackson et al. (1978), who directly influenced performance of rats preexposed to inescapable shock during the shuttlebox test through manipulation of shock intensity. The most likely basis for this effect is considered to be an increase in activity from the depressed level produced by exposure to inescapable shock. The basis for this increase in activity is an increase in appetitive drive produced by water deprivation. Even when water deprivation is limited to inescapable shock exposure, the resulting activity increase appears sufficient to prevent the inactivity contributing to subsequent shock-escape impairment.
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|Author:||Stromberg, Michael F.; Bersh, Philip J.; Whitehouse, Wayne G.; Neuman, Paul; Mongeluzzi, Donna L.|
|Publication:||The Psychological Record|
|Date:||Mar 22, 1997|
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