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At least 19 recordsLinked to original sources
PubMed1976

Some behavioral effects of morphine, naloxone and nalorphine in the squirrel monkey and the pigeon.

Morphine, naloxone and nalorphine were studied for their effects on the performance of squirrel monkeys and pigeons responding under multiple fixed-interval (FI), fixed-ratio (FR) schedules of food presentation. Morphine generally produced only dose-related decreases in responding in both monkeys and pigeons; monkeys were 10 times more sensitive to morphine than pigeons. The only effect of lower doses of naloxone (0.01-1 mg/kg, monkeys; 1-10 mg/kg, pigeons) was to increase FI responding in some pigeons. Higher doses of naloxone (10-56 mg/kg), produced gross disturbances such as tremors and vomiting and decreased FI and FR responding of both monkeys and pigeons. Nalorphine had strikingly different effects on the behavior of the two species. In the pigeons, nalorphine consistently increased both FI and FR response rates at doses from 0.3 to 10 mg/kg and decreased responding only at doses of 30 to 100 mg/kg. Nalorphine did not increase responding at any dose in the monkeys and the pigeons, nalorphine was only one-tenth as potent as naloxone in antagonizing the effects of morphine on FI and FR responding. Decreasing response rates caused by nalorphine appeared to limit further its usefulness as a morphine antagonist. Antagonism of the rate-decreasing effects of morphine on FI and FR responding occurred over a narrower range of doses with nalorphine than with naloxone, especially in monkeys.

Animals↗
PubMed1976

Sigma effects of nalorphine in the chronic spinal dog.

The effects of graded doses of nalorphine and morphine were studied in nondependent chronic spinal dogs. Morphine and low doses of nalorphine produced behavioral changes characterized by indifference, whereas the largest dose of nalorphine produced canine delirium indistinguishable from that produced by SKF-10, 047 or cyclazocine. Nalorphine depressed the flexor reflex; however, a plateau was observed. The data suggest that nalorphine is a partial agonist of the kappa type and a sigma agonist in addition to being a competitive antagonist at the mu receptor, and further, that the dysphoric and hallucinogenic effects of nalorphine-like drugs are due to their sigma activity.

Animals↗
PubMed1977

Pentazocine, cyclazocine, and nalorphine as discriminative stimuli.

Pentazocine, cyclazocine, and nalorphine are narcotic antagonists that also have analgesic activity of their own. The present investigation compared the stimulus properties of these three drugs in rats. Each drug was used as a discriminative stimulus for a separate group of rats. Depression of one lever resulted in food reinforcement following the administration of drug, and the opposite lever was reinforced after saline. Each drug readily acquired control of discriminated responding. The specific narcotic antagonist, naloxone, which antagonizes many of the effects of pentazocine, cyclazocine, and nalorphine, also antagonized the discrimination of these drugs. Stimulus generalization tests to each other narcotic antagonist, d-amphetamine, morphine, and LSD, showed that each narcotic antagonist has highly specific stimulus properties. Clear generalization occurred only to pentazocine and cyclazocine in the nalorphine-saline group, but neither cyclazocine nor pentazocine generalized to nalorphine.

Animals↗
PubMed1977

An investigation of nalorphine and perphenazine as negative reinforcers in an escape paradigm.

Rhesus monkeys were trained to self-administer morphine intravenously at dose levels sufficient to develop physical dependence. The monkeys were then trained to press a lever to escape a continuous infusion of the morphine antagonist, nalorphine. When saline was substituted for the nalorphine, escape responding extinguished. After morphine self-administration was eliminated, responding to escape from nalorphine was maintained in the postdependent monkeys, showing no difference from escape responding during morphine dependence. Finally, perphenazine was substituted for the nalorphine and the monkeys reliably escaped continuous infusions of this phenothiazine. The escape procedure appears useful for analyzing the aversive properties of drugs.

Animals↗
PubMed1978

Induction of alcohol withdrawal symptoms by nalorphine in chronic alcoholic patients.

The effect of nalorphine on eliciting symptoms of either alcohol or narcotic withdrawal was studied. Five male alcoholics were challenged with nalorphine and saline, both while sober and during alcohol ingestion. After nalorphine, pulse rate decreased in patients when sober, but increased when they were ingesting alcohol. Nalorphine administration resulted, during alcohol ingestion, but not in the sober state, in lacrimation, a symptom of narcotic withdrawal, in one patient, and in the following symptoms of alcohol or narcotic withdrawal in one or more patients: weakness, anorexia, insomnia, disorientation, and tremor. These findings suggest that morphine-like alkaloids play a role in the mediation of alcohol withdrawal symptoms.

Adult↗
PubMed1977

The effects of naloxone and nalorphine during the development of morphine dependence in rhesus monkeys.

A randomized and blind experimental design was used to study the effects of naloxone and nalorphine on the development of morphine dependence in monkeys. The results suggest: (a) that significant dose-related differences existed for combined numbers of withdrawal symptoms times frequency of occurrences; (b) that naloxone and nalorphine were qualitatively similar; (c) antagonists are more effective as dependence develops; (d) naloxone is approximately 10 times more potent than nalorphine, and (e) vomiting was the only withdrawal sign with which ED50s could be calculated. Dependence on morphine still increases up to 9 months after the commonly accepted 90-day stabilization period as measured by the ED50 for vomiting for naloxone.

Animals↗
PubMed1977

The effect of the narcotic antagonists naloxone, naltrexone and nalorphine on spinal cord C-fiber reflexes evoked by electrical stimulation or radiant heat.

C-fiber reflexes were recorded from an S1 ventral root in the acute decerebrate low spinal cat following stimulation of the ipsilateral superficial peroneal nerve or application of radiant heat to the metacarpel footpad. Naloxone when administered i.v. increased the electrically evoked C-fiber reflex to 158% (+/- 23.8% S.E.M.) of control 10 min after administration; whereas, naltrexone, 0.0025 mg/kg, increased the C-fiber reflex to 206 +/- 26.1% (S.E.M.) of control. Naloxone in a dose of 0.050 mg/kg increased the radiant heat evoked ventral root reflext to 161 +/- 19.5% of control. Nalorphine, 1 mg/kg, facilitated the electrically evoked C-fiber reflex to 282 +/- 75% of control. These findings that naloxone and naltrexone facilitated these reflexes in doses too small to have non-specific excitatory effects and that nalorphine facilitated the C-fiber reflex at a dose level that is depressant to the flexor reflex in the chronic spinal dog are consistent with a hypothesis that these effects are due to antagonism of a naturally occurring opiate-like inhibitory substance.

Action Potentials↗
PubMedDate not supplied

The sensitivity of the respiratory center and some circulatory and subjective responses after nalorphine and naloxone injections.

In five volunteers the sensitivity of the respiratory centre to carbon dioxide after naloxone and nalorphine injections was studied using "double blind" method and increments of doses. Alterations in the respiratory centre sensitivity were reflected by changes in respiratory minute volume, which was measured before and after drug injections, as well as after carbon dioxide stimulation. Comparison of results and their statistical verification showed that nalorphine alone causes respiratory depression and carbon dioxide stimulation is, beside the weak initial action, almost ineffective. Naloxone causes very small, if at all, respiratory depression and the respiratory centre answers efficiently to carbon dioxide stimulation.

Carbon Dioxide↗
PubMed1977

[The effect of nalorphine on analgesia induced by peripheral stimulation].

The blockade of effects induced by percutaneous peripheral stimulation were abolished by injection of an opiate antagonist as nalorphine. Our results lead to the hypothesis that central and peripheral stimulations act by the same mechanism in producing blockade of noxious impulses. One may suggest that peripheral stimulations induce release of endogenous morphine-like substances which in turn give descending inhibition.

Analgesia↗
PubMed1979

[Comparison of the effects of analgesia-producing peripheral and central stimulations in cats. Effect of nalorphine (author's transl)].

The effects of weak intensity percutaneous peripheral stimulations (SPPc) on the transmission of nociceptive messages induced by stimulation of the dental pulp have been studied on anaesthetized cats. 1. The jaw opening reflex (ROG) and the evoked potentials in the thalamic center median (CM), by stimulation of the dental pulp, disappear after a mean of 30 min after the start of SPPc. 2. These effects are analogous to those obtained by stimulation of the periaqueductal gray matter (St.GC) or by I.V. morphine injection. 3. The I.V. injection of the morphine antagonist (Nalorphine) blocks both the effects of the SPPc and those of the St.GC. 4. The authors put forth the hypothesis of a common mechanism of action of the SPPc and the St.GC which, through the liberation of endogenous morphinomimetic substances, would activate descending inhibitor impulses.

Animals↗
PubMed1977

Effects of morphine, methadone, nalorphine and naloxone on responding under schedules of electric shock titration.

Under two titration schedules, responses of squirrel monkeys adjusted the intensity of a continuous electric shock. In one schedule, responses produced food pellets but also increased a shock intensity which otherwise was decreased at a fixed rate (punishment titration). In another schedule, responses decreased a shock intensity which otherwise was increased at a fixed rate (escape titration). Responding maintained under the punishment titration schedule was only decreased by morphine, methadone, nalorphine and naloxone. This decrease in response rate was associated with a decrease in intensity of continous electric shock. Comparable rates of responding maintained under the escape titration schedule were either unaffected or increased over the same dose range of the same drugs. These effects on rate of responding were associated with either no effect or a slight decrease in intensity of continuous electric shock. When control rate of responding under the escape titration schedule was then increased by requiring five responses to decrease shock intensity, morphine, but not d-amphetamine, decreased responding at doses which had no effect or even increased responding when only one response was required to decrease shock intensity. These findings indicate that titration schedules are not always useful for studying the analgesic effects of drugs, but that specific effects of drugs are determined by specific details under which responding is maintained.

Analgesics↗
PubMed1978

The discriminative stimulus properties of cyclazocine: generalization studies involving nalorphine, morphine and LSD.

Rats learned to discriminate cyclazocine (2 mg/kg, i.p.) from saline using a two-lever operant (FR-4) procedure within 10 sessions under each drug condition. The cyclazocine discriminative stimulus (DS) was both dose- and time-related, being antagonized by naloxone at doses approximately 80 times that necessary to block the discriminative stimulus effect of morphine. Cyclazocine also generalized to nalorphine, but not to morphine, pentazocine or LSD. These data suggest that cyclazocine produced DS control of behavior by acting at CNS sites different from those affected by morphine or LSD.

Animals↗
PubMed1978

Nalorphine-like properties of some 2,3-dimethyl-3-arylpiperidines.

A number of N-substituted 2,3-dimethyl-3-arylpiperidines having an m- or p-arylhydroxyl were prepared and evaluated for analgesic agonist and antagonist properties. The diastereomeric N-allyl and N-cyclopropylmethyl derivatives behaved as pure potent antagoinists. Substitution of the arylhydroxyl from the meta to the para position resulted in a net fall of the antagoinist activity.

Analgesia↗