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PubMed1980

Interactions between narcotic agonists, partial agonists and antagonists evaluated by schedule-controlled behavior.

The effects of morphine, butorphanol, cyclazocine, ketocyclazocine, ethylketocyclazocine, and SKF-10,047 were tested, alone and in conjunction with naloxone or naltrexone, in rats responding under a fixed-interval, 5-min schedule of food presentation. Except for naloxone and naltrexone, all of the drugs decreased the average rate of responding in a dose-dependent manner. The rate-decreasing effects of morphine were markedly antagonized by naltrexone, while the effects of SKF-10,047 or high doses of cyclazocine were not antagonized by naltrexone or naloxone. Naltrexone and naloxone were able to antagonize the effects of butorphanol, ketocyclazocine, ethylketocyclazocine and low doses of cyclazocine, but these drugs were considerably more difficult to antagonize than was morphine. Thus, the interactions between these drugs and the narcotic antagonists allow the classification of the drugs into three groups, based on a marked shift, a moderate shift or no shift in the dose-response curve. This classification is consistent with the hypothesis of Martin et al., (Journal of Pharmacology and Experimental Therapeutics, 197: 517-532, 1976) regarding distinct receptors for morphine and related drugs (mu agonists), ketocyclazocine and ethylketocyclazocine (kappa agonists) and SKF-10,047 (sigma agonist).

Analgesics, Opioid↗
PubMed1978

Effects of d-amphetamine, monomethoxyamphetamines and hallucinogens on schedule-controlled behavior.

The effects of 16 drugs were studied in rats responding under fixed-ratio (FR 30) and fixed-interval (FI 2 minute) schedules of food presentation. The drugs tested included lysergic acid diethylamide (LSD), dimethyltryptamine, mescaline, d-amphetamine and 12 methoxylated amphetamines. All of the drugs decreased the average rates of responding under both schedules, but their potencies varied widely. For example, with LSD, the most potent drug tested, doses of 0.1 to 0.3 mg/kg were sufficient to reduce responding while with dimethyltryptamine and mescaline, doses of 10 to 30 mg/kg were required to clearly reduce responding. For the 12 drugs which are known to produce hallucinogenic effects, their potencies in reducing responding were positively correlated with their reported potencies in producing these subjective effects in humans. Although all of the drugs decreased the average rates of responding, alterations in the patterns of responding under the FR and FI schedules varied among the drugs. Analysis of responding under the FI schedule indicated that d-amphetamine, m-methoxyamphetamine, p-methoxyamphetamine, LSD and 3,4-methylenedioxyamphetamine generally increased the low rates of responding occurring at the beginning of each interval and decreased the high rates of responding occurring later in each interval (rate-dependent effects). The other drugs generally decreased responding throughout the interval. These results are discussed in terms of the known neurochemical effects of these drugs.

Amphetamines↗
PubMed1983

Effects of picenadol and its agonist and antagonist isomers on schedule-controlled behavior.

The effects of picenadol and its (+)- and (-)-isomers were determined on the responding of pigeons under a multiple fixed-ratio (FR) 50-response, fixed-interval (FI) 5-min schedule of grain presentation. Picenadol decreased responding in both schedule components as a function of dose (0.64-10 mg/kg). Naloxone shifted to the right the picenadol dose-effect curve in the FR component (2.8-fold), but had little effect on the dose-effect curve for FI responding. Similarly, the (+)-isomer decreased responding in both schedule components, but naloxone was only able to shift to the right the dose-effect curve for the (+)-isomer on FR responding (2-fold). The effects of the (+)-isomer on FI responding were not affected by naloxone. The (-)-isomer decreased responding at high doses (20 and 40 mg/kg) and this effect was not antagonized by naloxone. The dose-effect curves for the (-)-isomer were shifted markedly to the left in animals maintained on daily doses (30 or 60 mg/kg p.o.) of methadone. Low doses (2.5-20 mg/kg) of the (-)-isomer antagonized the behavioral suppressant effects of 5 mg/kg of l-methadone. The (+)-isomer, but not the (-)-isomer, antagonized the complete behavioral suppression produced by 0.05 mg/kg of oxotremorine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

Effects of intraventricular morphine and enkephalins on schedule-controlled behavior in nondependent, morphine-dependent and postdependent rats.

The effects of intraventricular morphine and the metabolically stable enkephalin analogs, D-ala2-leu- and D-ala2-met-enkephalinamide, were compared on food-reinforced operant responding in nondependent, morphine-dependent and postdependent rats. Dependence was induced and maintained by scheduled access to 0.05% morphine solution for 10 min every 6 hr for at least 8 weeks before testing. In nondependent animals, the lowest dose of the three drugs increased responding, whereas higher doses, i.e., 0.3 to 3.9 micrograms of morphine and 0.1 to 30 micrograms of the two enkephalins, produced graded decreases in responding. On a molar basis, morphine was 2 to 3 times more potent than the enkephalins in decreasing response rate. Naloxone (0.1 and 1.0 mg/kg) competitively antagonized the rate-decreasing effect of all three compounds. However, chronic morphine treatment produced varying changes in the effects of morphine and the enkephalins. Morphine-dependent rats were tolerant to the rate-decreasing action of morphine, whereas the rate-decreasing effect of D-ala2-met-enkephalinamide was unchanged and that of D-ala2-leu-enkephalinamide was enhanced. Protracted changes in the rate-decreasing effect of morphine, but not the enkephalins, were evident in postdependent animals that were tested 5 weeks after withdrawal from morphine. Thus, the effects of morphine and the enkephalins on operant responding are differentially altered as a result of chronic morphine treatment. These results could reflect an allosteric interaction between the neuronal binding sites for morphine and the enkephalins.

Animals↗
PubMed1981

Acute and chronic effects of naltrexone and naloxone on schedule-controlled behavior of squirrel monkeys and pigeons.

Dose-effect curves were obtained for the influence of naltrexone, of naloxone and of morphine on lever-pressing responses of squirrel monkeys and key-pecking responses of pigeons maintained by food presentation during fixed-interval (FI) and fixed-ratio (FR) components of a multiple schedule. Morphine caused dose-related decreases in FI and FR responding, with complete suppression occurring after 3 mg/kg was administered to monkeys and after 10 mg/kg was administered to pigeons. Naltrexone doses as low as 0.03 mg/kg (monkeys) or 0.1 mg/kg (pigeons) and naloxone doses as low as 0.1 mg/kg (monkeys) or 1 mg/kg (pigeons) shifted morphine dose-effect curves by one or more log units to the right. The effects of a 3 mg/kg injection of morphine were blocked completely by naltrexone (0.1-0.3 mg/kg) injected up to 16 hr before morphine, but not by naloxone (0.3-1 mg/kg) injected more than 2 hr before morphine. Thus, naltrexone was 3 to 10 times more potent than naloxone as an antagonist of morphine and was longer acting. Given alone, only high doses of naltrexone or naloxone (10 mg/kg, monkeys; 56 mg/kg, pigeons) had pronounced actions; FR and FI responding were markedly decreased and vomiting often occurred. Repeated daily injections of these high doses of naltrexone or naloxone resulted in little or no tolerance. One to 6 months after termination of chronic treatment, dose-effect curves for naltrexone on FR and FI responding maintained by food presentation were shifted markedly to the left with the monkeys, but not with the pigeons.

Animals↗
PubMed1980

Peptides controlling behavior in Aplysia.

Figure 11 summarizes our present understanding of the relationships between the bag cells, the atrial gland, their respective peptides, the central nervous system, and reproductive behavior. There are some interesting aspects of the overall organization of the system. The three hormonal peptides (ELH and the two atrial gland peptides) have specific actions on the central nervous system not unlike what we are currently learning from mammalian systems (e.g., LHRH and TRH). ELH, in addition, has several specific peripheral targets, the details of which remain to be worked out. The fact that ELH and other hormones have multiple targets within the central nervous system as well as nonnervous peripheral targets raises the question of whether one or more different receptors exist for single hormone. We suggest that peptides larger than perhaps five residues may carry several "messages" or receptor binding sites encoded within the one molecule. Large peptides such as ELH could obviously have separate domains of charge distribution within the molecule, and these would have the advantage, over the classical small molecule transmitters, of activating a variety of very different targets. The atrial gland is a peripheral source of peptides with potent nervous system actions; this is reminiscent of peptides in mammals, e.g., substance P, gastrin, and somatostatin, all of which were initially isolated from the gut and which are now being found in and also have actions on the central nervous system. Such resemblances in the principles of organization between mammals and molluscs are constant reminders that neuropeptidergic systems are old tricks in the evolutionary bag and that what we learn from molluscs and other invertebrates about mechanisms and organization will likely apply to mammals.

Amino Acid Sequence↗