Neonatal low-level lead exposure in monkeys: locomotor activity, schedule-controlled behavior, and the effects of amphetamine.
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Animals↗
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Prior drug experience and effects of amphetamine on schedule controlled behavior.
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Animals↗
Effects of delta-9-THC and a water soluble ester of delta-9-THC on schedule-controlled behavior.
delta-9-Tetrahydrocannabinol (delta-9-THC) and one of its water soluble esters (SP-111) decreased the rates of responding by pigeons working under a variable interval 3-min schedule of food presentation, or a multiple fixed-ratio 30, fixed-interavl 5-min schedule of food presentation. delta-9-THC was 3-6 times more potent than SP-111 and had a faster onset of effects on behavior.
Animals↗
Effects of clozapine, chlorpromazine and diazepam upon adjunctive and schedule controlled behaviors.
Two twelve-animal groups of rats were trained to press a lever for food reinforcement under either a fixed ratio 20 (FR 20) or a fixed interval 2 min (FI 2 min) schedule. During the FI 2 min schedule a measure of adjunctive behavior (i.e., drinking) was taken. Each group was then administered various doses of chlorpromazine (2.5, 5.0, 10.0 mg/kg, P.O.), clozapine (2.5, 5.0, 10.0 mg/kg, P.O.) or diazepam (5.0, 10.0, 15.0 mg/kg, P.O.) in a random order. All three drugs reliably reduced FR 20 response rates in a dose dependent manner, but chlorpromazine and clozapine were more potent in this regard. Chlorpromazine reduced FI 2 min responses rates especially in the terminal portions of the fixed intervals while diazepam generally elevated rates primarily in the min-portion of the interval. Clozapine produced a less defined effect on overall responding. All three drugs affected index of curvature. Only chlorpromazine was able to reliably reduce occurrence of adjunctive behavior and reinforcements.
Animals↗
Stereoselective effects of 1-(2,5-dimethoxy-4-methylphenyl)-2-aminopropane (DOM) on schedule-controlled behavior.
The effects of R(-)-, S(+) and R, S-1-2-5-dimethoxy-4-methylphenyl)-2-Aminopropane (DOM) were studied using rats responding under a fixed interval two-min schedule of food presentation. All three drugs decreased average rates of responding in a dose-related manner, with R -DOM being five to six times more potent than S-DOM increased the low response rates occurring at the beginning of the fixed interval and decreased the higher response rates occurring at the end of the interval (rate-dependent effects). These results are discussed in terms of the stereoselective metabolism of DOM and of the structural similarities between R-DOM and the behaviorally active isomer of LSD.
DOM 2,5-Dimethoxy-4-Methylamphetamine↗
Effects of combinations of phencyclidine and pentobarbital on schedule-controlled behavior in the squirrel monkey.
Three squirrel monkeys trained on a variable interval schedule of food presentation were used to examine the interaction between phencyclidine (PCP) and pentobarbital (PB). First, dose-response curves for each drug given alone were obtained. PCP caused small response rate increases at low doses, and a dose-dependent decrease in responding at higher doses. PB caused only dose-dependent decreases in responding. The PB dose-response curve was then redetermined in the presence of four doses of PCP. Little support was found for the hypothesis that PCP enhances the depressant properties of PB. In fact, most dose combinations caused less disruption of responding than expected from simple addition of the effects of each drug given alone. These results are discussed in terms of species differences, measurement of different dipendent variables and rate-dependency.
Animals↗
Effects of clozapine, chlorpromazine and haloperidol on schedule-controlled behavior.
The effects of clozapine, chlorpromazine, and haloperidol were determined in mice and pigeons responding under a multiple fixed-ratio 30, fixed-interval 600 sec schedule of food presentation. In both species, low doses were without effect and moderate to high doses of all three antipsychotics decreased responding. In contrast to other behavioral tests used to predict antipsychotic activity, clozapine was equipotent or more potent than chlorpromazine in decreasing responding under the multiple fixed-ratio 30, fixed-interval 600 sec schedule. The order of potency observed in the mouse was: haloperidol greater than chlorpromazine greater than or equal to clozapine. The order of potency in the pigeon was: haloperidol greater than clozapine greater than chlorpromazine. In mice and pigeons, the rate of responding under the fixed-ratio component was decreased at lower than, or the same doses of clozapine as that required to decrease fixed-interval responding. However, in both species, chlorpromazine and haloperidol decreased fixed-interval responding at lower doses or the same dose as that required to decrease fixed-ratio responding.
Animals↗
Effects of phenytoin, phenobarbital, and valproic acid, alone and in selected combinations, on schedule-controlled behavior of rats.
The present study examined the effects of phenytoin (20, 30, 40, and 50 mg/kg), phenobarbital (10, 20, 30, and 40 mg/kg), and valproic acid (80, 120, 160, and 240 mg/kg), and those of phenobarbital (10 and 30 mg/kg) combined with phenytoin (20, 30, and 40 mg/kg) or valproic acid (80, 120, and 160 mg/kg), on the lever pressing of rats maintained under fixed-ratio and interresponse-time-greater-than-t schedules of food delivery. High doses of each individual drug significantly decreased mean group response (and reinforcement) rate under the fixed-ratio schedule. No dose of an individual agent significantly affected mean group response rate under the interresponse-time-greater-than-t schedule, although high doses of phenobarbital and valproic acid significantly reduced the mean group reinforcement rate under this schedule. When given in combination, phenobarbital and phenytoin and phenobarbital and valproic acid significantly reduced response (and reinforcement) rate under the fixed-ratio schedule and reinforcement rate under the interresponse-time-greater-than-t schedule. These reductions did not significantly differ in magnitude from those predicted by an additive model of drug interaction.
Animals↗
Investigation of the actions of the benzodiazepine antagonists Ro 15-1788 and CGS 8216 using the schedule-controlled behavior of rats.
Ro 15-1788 and CGS 8216 antagonise many of the pharmacological effects of benzodiazepines but both of these compounds have also been shown to exert behavioral effects when administered alone. In the present study the effects of Ro 15-1788 and CGS 8216, alone and in combination with diazepam and with the benzodiazepine receptor ligand zolpidem, were investigated. Diazepam and zolpidem produced dose-related decreases in rates of food-reinforced lever-pressing maintained by a fixed-ratio (FR 10) schedule. CGS 8216 also reduced response rates although Ro 15-1788, at several doses, produced small, but statistically significant, increases in responding. When the diazepam and zolpidem dose-response curves were re-established in the presence of a dose of Ro 15-1788 or CGS 8216 the depressant effects of the higher doses were antagonised. However, neither diazepam nor zolpidem blocked the rate reducing effect of CGS 8216 which may not therefore be due to an action at benzodiazepine receptors.
Animals↗
Cholecystokinin potentiates the rate-decreasing effects of morphine on schedule-controlled behavior in rats.
In one component of a multiple schedule, responding (licking in rats) was reinforced under a fixed-ratio (FR 50) schedule of water presentation. In the other component, responding had no programmed consequences (timeout). Each session consisted of four 10-min timeout components alternating with four FR components. In general, increasing cumulative doses of morphine (3.2-18 mg/kg) produced a dose-dependent decrease in the overall rate of responding. In one subject, cholecystokinin (CCK) alone (10-32 micrograms/kg) produced dose-dependent decreases in rate in the first component, while in the other two subjects relatively little decrease in rate occurred. When these doses of CCK were given as a pretreatment before morphine, the decrease in overall response rate was greater than that found with morphine alone. This interaction was most noticeable at the lowest dose of morphine where CCK produced a dose-dependent "potentiation" of the rate-decreasing effects. Although the potentiation of CCK was not as evident at the intermediate doses of morphine, there were instances in which the rate-decreasing effects produced by the combination were greater than those expected from addition of the effects of CCK and morphine alone. In contrast, when naltrexone (1 mg/kg) was given as a pretreatment, little or no rate-decreasing effects were produced by the cumulative doses of morphine. Furthermore, pretreatment with naltrexone and the administration of a higher dose range of morphine indicated the dose-effect curve for morphine had shifted approximately 3/4 log-units to the right.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effects of terminating chronic phencyclidine on schedule-controlled behavior in rats.
Six rats were trained to respond under a multiple fixed-ratio 30, fixed-interval 3-min schedule for food presentation. Acute administration of phencyclidine (0.1-3.2 mg/kg, IP) produced decreases in fixed-ratio response rates at doses above 0.3 mg/kg, but fixed-interval response rates were only decreased at the highest dose. However, the pattern of fixed-interval responding (as evidenced by quarter-life values) was affected at doses above 0.3 mg/kg. Osmotic minipumps were implanted, SC, which infused saline (2 rats) or phencyclidine (4 rats, 10.0 mg/kg/day) for 10 days, and then removed. Daily behavioral sessions were conducted during infusions and for 10 days afterwards. The effects of phencyclidine infusions on fixed-ratio responding were variable. Fixed-interval response rate and quarter-life values were only modestly affected during drug infusion. All three parameters were markedly affected upon cessation of chronic phencyclidine dosing, but there did not appear to be differential effects between the schedule components. No effects on responding were observed during or after saline infusions.
Animals↗
Butorphanol's efficacy at mu and kappa opioid receptors: inferences based on the schedule-controlled behavior of nontolerant and morphine-tolerant rats and on the responding of rats under a drug discrimination procedure.
The purpose of the present investigation was to characterize the mu agonist and kappa antagonist effects of the mixed opioid agonist/antagonist butorphanol. To this end, the effects of butorphanol were examined: 1) alone and in combination with the kappa agonist bremazocine in nontolerant and morphine-tolerant rats responding under a fixed-ratio 30 (FR30) schedule of food presentation, and 2) in rats trained to discriminate 10 mg/kg morphine from saline. Prior to the induction of morphine tolerance, morphine, bremazocine and butorphanol produced dose-dependent decreases in rate of responding under the FR30. In these nontolerant rats, butorphanol failed to antagonize bremazocine's rate-decreasing effects. During the chronic morphine regimen, the dose-effect curve for morphine was shifted to the right of its prechronic position by approximately 0.9 log units, whereas the bremazocine curve was not altered substantially. The butorphanol dose-effect curve, in contrast, was shifted to the right and flattened such that doses which eliminated responding in nontolerant rats, as well as doses approximately 1.0 log unit higher, had no effect on responding. In these morphine-tolerant rats, butorphanol produced a dose-dependent antagonism of bremazocine's rate-decreasing effects. In rats trained to discriminate morphine from saline, butorphanol substituted completely for the morphine stimulus. Unlike morphine, which produced its stimulus effects only at doses that decreased rate of responding, butorphanol substituted for the morphine stimulus at doses that had little or no effect on rate of responding.(ABSTRACT TRUNCATED AT 250 WORDS)
Analgesics↗
The effects of cocaine in combination with other drugs of abuse on schedule-controlled behavior in the pigeon.
The present experiment sought to provide information regarding the consequences of combining cocaine with other drugs of abuse. The effects of cocaine alone and in combination with d-amphetamine, caffeine, morphine or delta-9-tetrahydrocannabinol were determined in five male white Carneaux pigeons responding under a multiple fixed-ratio 30, fixed-interval 600 schedule (mult FR FI). Drug interactions were studied by redetermining the cocaine dose-response curve in the presence of various fixed doses of the other drugs. Under the mult FR FI schedule, when cocaine (1 to 10 mg/kg) was combined with inactive doses of d-amphetamine (0.1, 0.3, 1.0, and 1.8 mg/kg), caffeine (10, 30, and 100 mg/kg), morphine (0.3, and 1.0 mg/kg), and delta-9-tetrahydrocannabinol (0.1 mg/kg), the FR and FI response rate dose-response curves were not shifted relative to the cocaine-alone curves. When cocaine was combined with an active dose of a drug which decreased response rate when given alone (0.3 mg/kg delta-9-tetrahydrocannabinol and 3 mg/kg morphine), the position of the response rate dose-response curves shifted compared to the cocaine-alone curves. The most frequent and consistent outcome of these interactions can be described as less than or approximately equal to an effect-additive interaction. Thus, these data indicate that the potential consequences of coabusing cocaine with the drugs tested in the present experiment can most often be predicted from the effects of each drug when taken alone.
Animals↗
Acute effects of the organophosphate paraoxon on schedule-controlled behavior and esterase activity in rats: dose-response relationships.
The effects of acute intraperitoneal administration of paraoxon on behavioral and biochemical parameters were studied in male rats. Rats were trained to press a lever under an FR10 schedule of reinforcement. Rats were injected with 3 sublethal doses of paraoxon (0.5, 0.75, and 1.0 mg/kg) and performance was monitored for four days after exposure. Response rates were depressed significantly for days 1 and 2 with 0.75 and 1.0 mg/kg, but not 0.5 mg/kg, even though there was inhibition of brain and plasma cholinesterases at all doses. Performance recovered prior to brain AChE recovery. There was no clear-cut threshold of brain AChE inhibition required to yield performance deficits, nor was there a direct correlation between significant inhibition in peripheral enzymes which could serve as markers (plasma aliesterases, butyrylcholinesterase, non-iso-OMPA-sensitive cholinesterase, and hepatic aliesterases) and performance deficits, suggesting that other noncholinergic targets may play a role in OP-induced behavioral deficits.
Acetylcholinesterase↗
Effect of eseroline on schedule-controlled behavior in the rat.
Male Sprague-Dawley rats were trained to press a lever on a simple-alternation multiple fixed-ratio (FR) 20-response time-out (TO) schedule for water reinforcement. Twelve 5-min periods of FR reinforcement were each followed by a 5-min TO in which responding had no scheduled consequence. Doses ranging from 0.25 to 8 mg/kg of eseroline, the hydrolysis product of eserine and a potent analgesic agent with weak anticholinesterase activity, were administered SC immediately prior to a 120-min test session. Eseroline produced a dose-dependent monotonic decrease in the number of reinforcements, with significant effects at doses of 1, 2, 4 and 8 mg/kg and an ED50 of 2.5 (1.6-3.4) mg/kg. This behavioral disruption was characterized by a rapid onset of pausing (i.e., within 5 min postdosing) and a gradual recovery to normal baseline levels of responding over the remaining session time. The duration of the rate decreasing effects was dose-related with the highest dose having a mean duration of more than 60 min, which was longer than that of previous reports on antinociception produced by eseroline (less than 60 min). The coadministration of behaviorally inactive doses of the opiate antagonist naloxone (1 and 2 mg/kg, IP) with eseroline (2.5 mg/kg, ED50) antagonized the effects of eseroline on the operant behavior. The coadministration of behaviorally inactive doses of the muscarinic antagonist atropine with eseroline (2.5 mg/kg) did not affect eseroline's behavioral effect. These results suggest that the effects of eseroline on operant behavior is consistent with the effects of eseroline-induced antinociception, reported previously, and appears to be associated with the activation of opiate receptors, but not related to the stimulation of muscarinic receptors via its anticholinesterase activity.
Analgesics↗
Peripheral injections of vasopressin control behavior by way of interoceptive signals for hypertension.
The stimulus properties of peripheral injections of vasopressin were assessed using conditioned taste aversion techniques. Conditioned taste aversion induced by vasopressin was blocked by prior exposure to vasopressin but not to another aversive agent, apomorphine. Prior exposure to behaviorally equivalent doses of another hypertensive agent, angiotensin II, blocked also conditioned taste aversion induced by vasopressin and this effect was fully reciprocal, since prior exposure to AVP blocked the aversive effect of angiotensin II. The protection offered by prior exposure to angiotensin II was not due to an endogenous release of AVP since the aversive properties of angiotensin II were not blocked by administration of a specific antagonist of the vasopressor effects of vasopressin. These data suggest that the interoceptive cues which are responsible for the conditioned taste aversion induced by vasopressin are related to the hypertensive action of this peptide.
Angiotensin II↗
Effects of trialkyltins on the schedule-controlled behavior of the pigeon.
Male White Carneaux pigeons trained to respond for food under a multiple fixed-ratio fixed-interval schedule of reinforcement were given single injections of trimethyltin (TMT), or triethyltin (TET). A dose of 0.3 mg/kg TMT produced no effect on behavior, while a 1.0 mg/kg dose was a threshold dose and 1.75 mg/kg produced behavioral changes that persisted for months in some birds. TMT produced effects on responding under the multiple schedule at approximately the same doses that produce neuronal damage in the hippocampus and the brain stem of the pigeon. Higher doses given to untrained birds produced signs of extensive neurological damage. A dose of 1.0 mg/kg of TET decreased rates of responding under both schedule components three hours after administration, but behavior usually had recovered by the next day. Doses of 3.0 and 5.6 mg/kg had similar effects, but responding did not recover for several days. Some birds showed significant rate increases, especially under the fixed-interval component several days to several weeks after TET administration. Doses greater than 10 mg/kg TET were lethal. Dose-effect curves for the effects of d-amphetamine, chlorpromazine and morphine on responding under the multiple schedule were determined for some birds before and one month after 1.0 and 1.5 mg/kg of TMT. TMT shifted the dose-effect curve for d-amphetamine to the right, but it did not produce systematic changes in the dose-effect curves for morphine and chlorpromazine.
Animals↗
Short-term effects of paraoxon and atropine on schedule-controlled behavior in rats.
The effects of lethal (2.0 mg/kg) and high sublethal (1.3 mg/kg) dosages of the organophosphate acetylcholinesterase (AChE) inhibitor paraoxon on FR10 performance rate was determined 1 and 2 days after intoxication. The lethal doses were antidoted with either centrally acting atropine sulfate (AS), or atropine methyl bromide (AMB) or atropine methyl nitrate (AMN), both quaternary salts and not expected to act centrally. AChE inhibition in the brain was about 35-60% on the second day after treatment. AS yielded a small transient depression in performance, while AMB and AMN yielded severe deficits, with incomplete recovery. Performance was depressed by 1.3 mg/kg paraoxon by 52% and 34% on days 1 and 2, respectively, while performance was more greatly depressed by the lethal dose, especially with the noncentrally acting antidotes: AS, 67 and 48%; AMB, 81 and 55%; AMN, 91 and 78%. However, a low dose of AS with 2 mg/kg paraoxon resulted in very severe, nonrecovering deficits. A lethal dose of the nonpersistent anti-AChE eserine sulfate, antidoted with a low dose of AS, yielded no deficits. Thus, a high level, acute intoxication with paraoxon yields behavioral deficits which are attenuated by high levels of a centrally acting muscarinic receptor antagonist. The paraoxon-induced performance deficits or their recovery do not correlate directly with AChE inhibition.
Acetylcholinesterase↗