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P Schnur

Publications and source records attributed to P Schnur.

At least 19 recordsLinked to original sources
PubMed2000

Malignant fibrous histiocytoma arising in a thoracotomy scar.

Malignant fibrous histiocytoma arises most commonly de novo and rarely from sites of chronic inflammation. The authors present a case of malignant fibrous histiocytoma arising in a thoracotomy hypertrophic scar. The patient required large local excision of the tumor down to and including the muscle layer with postoperative radiation treatment. Factors associated with the occurrence of this sarcoma are discussed along with salient management principles.

Cicatrix, Hypertrophic↗
PubMed1994

Context-specific sensitization to naloxone-precipitated withdrawal in hamsters: effect of pimozide.

Three experiments were conducted to investigate the development of context-specific sensitization to naloxone-precipitated withdrawal in hamsters. In Experiment 1, animals in group M/S were given morphine (15 mg/kg) injections in a distinctive environment and saline in the home cage. Animals in group S/M were given saline in the distinctive environment and morphine in the home cage, and animals in group S/S were given saline in both environments. All groups were challenged subsequently with naloxone (0.4 mg/kg) in the distinctive environment and then observed for signs of opiate withdrawal. The results showed that group M/S gave more naloxone-precipitated withdrawal signs than each of the other groups, which did not differ from one another. Experiment 2 was designed to test the effect of pimozide on context-specific sensitization to naloxone-precipitated withdrawal. The design was similar to that of Experiment 1 but group P/M/S, which received an injection of pimozide (0.5 mg/kg) 4 h prior to morphine, was added. The results indicated that context-specific sensitization developed as in Experiment 1, except among animals treated with pimozide. Experiment 3 was designed to determine whether pimozide interferes with the development or the expression of context-specific sensitization. Six groups, differing in the frequency and timing of the pimozide injection, were employed. The results indicated that pimozide interfered with context-specific sensitization, whenever it was given. It is concluded that pimozide interferes with the expression of context-specific sensitization, although a separate effect on the development of sensitization is not ruled out.

Animals↗
PubMed1992

Conditioned morphine withdrawal in the hamster.

Conditioned withdrawal among golden Syrian hamsters was studied in two experiments. In experiment 1, morphine-pelleted (75 mg) hamsters were observed for signs of withdrawal (wet-dog shakes, etc.) before and after a naloxone (1 mg/kg) injection that was administered in a distinctive environment. Withdrawal signs that occurred in the distinctive environment before the naloxone injection were defined as anticipatory conditioned withdrawal responses. Two, 9, and 30 days following pellet removal, retention of conditioned withdrawal responding was assessed in the distinctive environment before and after a saline injection. Results indicated that: a) withdrawal intensity was a direct function of the number of implanted pellets; b) conditioned withdrawal occurred among animals withdrawn in the distinctive environment, but not among those withdrawn in the home cage; c) conditioned withdrawal was a nonmonotonic function of precipitated withdrawal intensity; d) conditioned withdrawal was evident up to 30 days after pellet removal. In experiment 2, conditioned withdrawal was extinguished by repeated exposure to the distinctive environment in the absence of precipitated withdrawal. It was concluded that environmental stimuli associated with the absence of morphine (i.e., precipitated withdrawal) elicit conditioned withdrawal. The results are compared to similar findings in rats and humans.

Animals↗
PubMed1992

Conditioned withdrawal in environments associated with the presence or absence of morphine.

An experiment designed to compare conditioned withdrawal in environments associated with the presence or absence of morphine was conducted in hamsters. For some animals, morphine administration was paired with distinctive environmental cues. For other animals, naloxone-precipitated withdrawal was paired with the distinctive environmental cues. For still other animals, naloxone-precipitated withdrawal and the distinctive environmental cues were unpaired. Following 12 days of training, animals were observed for signs of withdrawal (e.g., wet-dog shakes, etc.) in the distinctive environment following vehicle injections. Results indicated that more conditioned withdrawal responses occurred in the environment paired with the absence of morphine (naloxone-precipitated withdrawal) than in the environment paired with morphine administration.

Animals↗
PubMed1992

Effects of diurnal phase and pimozide on cholecystokinin-elicited hypoactivity in the hamster.

Locomotor activity in golden Syrian hamsters was measured following IP injections of cholecystokinin (CCK; 25 micrograms/kg) and pimozide (0.5 mg/kg), the dopamine receptor antagonist. In addition, animals were tested during either the dark or light phase of the diurnal cycle in either dark or light running wheel environments. Results indicated that CCK-elicited hypoactivity was blocked by pimozide and that the effect of CCK was evident only among animals tested during the light phase of the daily cycle. Ambient lighting conditions in the test environment did not modify the drug effects. Independently of any drug effect, locomotor activity was affected by diurnal phase and ambient lighting in the test environment. Animals were more active when tested during the dark phase than during the light phase and locomotor activity was higher under dark than under light ambient conditions. It is concluded that diurnal phase modulates CCK's effect on hamster locomotion and that CCK's effect on locomotion is mediated, in part, by dopaminergic mechanisms.

Animals↗
PubMed1992

Blocking naloxone-precipitated withdrawal in rats and hamsters.

Three experiments studied the effects of putative antagonists of opiate withdrawal in hamsters and rats. In Experiment 1, the calcium channel antagonists verapamil (20 mg/kg) and nifedipine (20 mg/kg) failed to antagonize naloxone (1 mg/kg)-precipitated withdrawal in hamsters implanted with two 75-mg morphine pellets, whereas clonidine (0.4 mg/kg), the alpha 2-adrenergic agonist, blocked most withdrawal signs. In Experiment 2, clonidine (0.4 mg/kg) and verapamil (20 mg/kg) were tested against naloxone-precipitated withdrawal in hamsters made acutely dependent by a single injection of morphine (15 mg/kg). As in Experiment 1, clonidine but not verapamil was effective. In Experiment 3, the effects of verapamil on naloxone-precipitated withdrawal were studied in morphine-pelleted rats and hamsters. In rats implanted with two morphine pellets, verapamil (20 mg/kg) reversed naloxone-precipitated withdrawal. By contrast, in hamsters implanted with either one or two morphine pellets neither of two doses of verapamil (20 and 30 mg/kg) was effective. These results are discussed in terms of species' differences in sensitivity to calcium channel blockers.

Animals↗
PubMed1991

Effects of cholecystokinin on morphine-elicited hyperactivity in hamsters.

The effects of the octapeptide cholecystokinin (CCK) on hamster locomotor activity were investigated in three experiments. In Experiment 1, the effect of CCK (25, 50, 75 micrograms/kg) on morphine (2.5 mg/kg)-elicited hyperactivity was studied. Results indicated that CCK antagonized morphine-elicited hyperactivity and that CCK alone elicited hypoactivity. There were no effects of dose of CCK. In Experiment 2, the effects of intraperitoneal (IP) and subcutaneous (SC) routes of administration of CCK (25 micrograms/kg) on locomotor activity were studied. Compared to saline controls, CCK induced hypoactivity that was of greater magnitude and of longer duration when administered IP than SC. Experiment 3 was designed to replicate the route of administration effect observed in Experiment 2 and to determine whether sensitization to CCK-induced hypoactivity develops over the course of a few injections. Results indicated that CCK-induced hypoactivity was greater after IP than SC administration but that sensitization was not detectable. It is concluded that CCK antagonizes morphine-elicited hyperactivity in the hamster by acting, in part, independently of morphine to produce opposite behavioral effects.

Animals↗
PubMed1991

Acute morphine dependence in the hamster.

Two experiments investigated naloxone-precipitated withdrawal following a brief course of morphine administration in hamsters. In Experiment 1, observable withdrawal symptoms (e.g., wet-dog shakes) were elicited by two doses of naloxone (0.4 and 1.0 mg/kg) following four and eight daily injections of morphine (15 mg/kg), a regimen that replicated previous studies in our laboratory using a locomotor activity paradigm. At the lower dose of naloxone, the frequency of withdrawal signs was greater after eight than after four morphine injections. In Experiment 2, observable withdrawal symptoms were elicited by the same two doses of naloxone, 70 min after a single morphine injection. These results suggest that acute dependence in the hamster, as in other species, beings to develop with the first morphine exposure.

Animals↗
PubMed1990

Effects of U50,488H on locomotor activity in the hamster.

Two experiments investigated the effects of the specific kappa opiate agonist, U50,488 on locomotor activity in the golden Syrian hamster. In Experiment 1, the effects of U50,488 were found to be dose-related, with a 1 mg/kg dose eliciting hyperactivity and a 10 mg/kg dose eliciting hypoactivity. In Experiment 2, the dual effects of U50,488 on locomotor activity were shown to be naloxone (1 mg/kg) reversible. It is suggested that the effects of U50,488 on activity are consistent with the reported dual opposing influences of kappa agonists in the substantia nigra pars compacta and pars reticulata.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1990

Morphine conditioned place preference in the hamster.

Two experiments investigated the ability of morphine to produce a conditioned place preference in the hamster. In Experiment 1, it was found that a 15 mg/kg dose of morphine produced a conditioned place preference after eight conditioning trials. In addition, naloxone (0.4 mg/kg blocked the development of the morphine-conditioned place preference and itself produced a conditioned place aversion after four conditioning trials. In Experiment 2, the effects of four doses of morphine (0, 2.5, 5 and 15 mg/kg) on the acquisition of a conditioned place preference were studied. Only the 15 mg/kg dose produced a significant place preference. Compared to similar findings in the rat, the present results indicate that a relatively high dose of morphine is required to produce a conditioned place preference in the hamster.

Animals↗
PubMed1989

Independent effects of morphine and apomorphine on stereotyped gnawing in the hamster.

Eight experiments were conducted to investigate the effects of apomorphine, a dopaminergic agonist, and of morphine, an opiate, on stereotyped behavior in the hamster. Animals were observed at two minute intervals for one hour and incidents of stereotyped gnawing, licking and sniffing were recorded using a time-sampling method. Both morphine and apomorphine produced dose-related increases in stereotyped gnawing. A low dose of the opiate antagonist, naloxone (0.4 mg/kg), blocked morphine-induced gnawing but neither that dose nor higher doses of naloxone (1, 4 and 10 mg/kg) blocked apomorphine-induced gnawing. A low dose of the dopaminergic antagonist, haloperidol (0.05 mg/kg), blocked apomorphine-induced gnawing but did not block morphine-induced gnawing. Further experiments indicated that morphine administration did not sensitize, or influence in any way, subsequent apomorphine-induced stereotyped behavior.

Animals↗
PubMed1988

Bombesin-induced grooming in the golden hamster.

Lateral cerebroventricular injection of the peptide bombesin (0.01-1.0 micrograms) promptly elicited excessive grooming and scratching behaviors in home-caged male and female golden hamsters. Bombesin-induced grooming persisted throughout a 60-min observation period at doses of 0.1-1.0 micrograms. Grooming with forepaws and mouth was more consistently increased than hindleg scratching behaviors. Dependence of this neuropeptide effect on grooming on muscarinic cholinergic activity was assessed by injecting scopolamine (0.001-1 mg/kg) intraperitoneally 15 min prior to 0.1 microgram bombesin. Excessive grooming induced by centrally administered bombesin was abolished by 0.1 and 1 mg/kg scopolamine, although basal level of grooming was not significantly affected. The findings indicate a cross-species generality of the dependence of bombesin-induced grooming on muscarinic cholinergic activity, and species-specific differences among rodents in the components of excessive grooming elicited by bombesin.

Animals↗
PubMed1988

Effects of stress on morphine-elicited locomotor activity in hamsters.

Two experiments were conducted to investigate the effects of stress on morphine-elicited locomotor activity in hamsters. In Experiment 1, half of the animals were habituated to handling and injection procedures (low-stress condition) and half were not (high-stress condition) prior to 6 days of testing with a low dose (2.5 mg/kg) of morphine. On the first test day, morphine elicited hyperactivity among habituated animals, whereas among nonhabituated animals morphine elicited hypoactivity. The effects of handling diminished across test days, so that on the last test day, morphine elicited hyperactivity in both habituated and nonhabituated animals. In Experiment 2, the effect of a noise stressor on activity elicited by three doses of morphine (2.5, 5.0, and 15 mg/kg) was investigated. Half of the animals were tested under conditions of low noise stress (70 dB), and half were tested under conditions of high noise stress (90 dB). Results indicated that the effects of each dose of morphine were potentiated in the high-stress relative to the low-stress condition. Both experiments demonstrated that environmental stressors can potentiate the response to exogenous opiate administration in hamsters. Moreover, the results are consistent with the hypothesis that stress induces the release of endogenous opioids which summate with exogenous opiates to determine the final effective dose.

Animals↗
PubMed1987

Naloxone reversal of morphine elicited hyperactivity.

When naloxone is administered during morphine elicited hyperactivity, hyperactivity is reversed and hypoactivity occurs in its place. The present experiment tested the hypothesis that this effect is the result of morphine induced supersensitivity to naloxone. Two groups of hamsters received equivalent pretreatment with 15 mg/kg morphine (Groups M/M and M/S) for three days while a third group received saline (Group S/S). During subsequent testing one group received a morphine injection (Group M/M) while the others received saline (Groups M/S and S/S) before being placed in running wheels for a three hour session. Two hours later half the animals in each group received an injection of 0.4 mg/kg naloxone and half received saline. Naloxone produced hypoactivity in animals running under the influence of morphine (Group M/M), but neither in those with an equivalent history of morphine pre-treatment (Group M/S), nor in saline controls (Group S/S). These results are inconsistent with the hypothesis under test, but congruent with a modified dual-action hypothesis.

Animals↗
PubMed1986

Evidence for an underlying opponent process during morphine elicited hyperactivity in the hamster.

Two experiments investigated the effects of naloxone on morphine elicited hyperactivity in the hamster. In Experiment 1, naloxone (0.4 mg/kg) administered two hours after morphine (15 mg/kg) produced sedation in animals running at high rates under the influence of morphine. Saline control animals running at comparable rates were unaffected by naloxone. In Experiment 2, naloxone administered two hours after morphine converted morphine elicited hyperactivity into sedation. These results are discussed in terms of a modified dual-action hypothesis which holds that morphine elicited hyperactivity masks an underlying opponent process.

Animals↗
PubMed1986

Cholecystokinin antagonizes morphine induced hypoactivity and hyperactivity in hamsters.

Three experimental replications were used to test the effects of three doses (25, 50 or 75 micrograms/kg) of cholecystokinin octapeptide (CCK-8) on morphine induced changes in activity. For each dose of CCK-8, running wheel activity of golden Syrian hamsters was monitored for three hours following a series of two injections. The first injection consisted of either saline or CCK-8, the second of either saline or morphine sulfate (15 mg/kg). Thus, in each replication four groups were created: Group SAL/SAL (n = 8) received two saline injections, Group CCK/SAL (n = 8) an injection of CCK-8 followed by an injection of saline, Group SAL/MS (n = 8) an injection of saline followed by an injection of morphine and Group CCK/MS (n = 8) an injection of CCK-8 followed by an injection of morphine. Results indicated that a 25 micrograms/kg dose of CCK-8 blocked the hypoactivity elicited by morphine 40-60 min after opiate injection, whereas a 75 micrograms/kg dose of CCK-8 blocked the hyperactivity elicited by morphine 80-100 min after opiate injection. These findings are consistent with previous reports that CCK-8 antagonizes the effects of opiate agonists on a variety of behaviors and is supportive of the hypothesis that endogenous CCK-8 may antagonize endogenous opioid peptides in the control of behavior.

Animals↗