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Biomedical subjects

L Shuster

Publications and source records attributed to L Shuster.

15 recordsLinked to original sources
PubMed1992

Phenobarbital-responsive episodic dyscontrol (rage) in dogs.

Episodic dyscontrol (rage) was diagnosed from the clinical history, electroencephalographic findings, and response to oral treatment with phenobarbital in 3 dogs. Clinical features included a mood change heralding aggressive incidents, explosive aggression directed at people or objects, and a postaggressive phase characterized by lethargy and lack of responsiveness. Abnormal electroencephalographic findings included spike activity in the temporal recordings. All 3 dogs responded well to anticonvulsant medication with phenobarbital.

Aggression↗
PubMed1992

Hepatic morphologic and biochemical changes induced by subacute cocaine administration in mice.

The initial event and site of cocaine-induced hepatic injury have not been elucidated. In an attempt to identify the minimal effective dose and the site of injury, we have examined the livers of mice exposed to small daily doses of cocaine, using morphological and biochemical methods. All doses of cocaine greater than 5 mg/kg were able to cause significant elevation of serum glutamic pyruvic transaminase. Light microscopy revealed a progression of centrilobular necrosis as the dose increased from 10-30 mg/kg. The initial morphologic changes observed prior to necrosis included aggregation of intermediate filaments and dilation of rough endoplasmic reticulum with loss of ribosomes. Immunohistochemistry, using antibodies to cytokeratins, showed staining of individual hepatocytes in livers from cocaine-treated animals but not in controls. In contrast to earlier reports, we found little, if any, disruption of mitochondria. In vitro, the direct application of cocaine, norcocaine, and N-hydroxynorcocaine on isolated mitochondria had no effect on the ADP:O or respiratory control ratios, at concentrations up to 2.0 mM. Our studies demonstrate that any early cellular alterations in cocaine-induced hepatic injury are manifested in intermediate filaments and endoplasmic reticulum with no evidence of mitochondrial involvement.

Alanine Transaminase↗
PubMed1977

Sensitization to cocaine stimulation in mice.

Repeated administration of cocaine to B6AF1/J mice increased their running response to 20 mg/kg cocaine as much as four-fold over the response to the first injection. After four daily injections, the extent of the increase was proportional to the dose of cocaine that was used for pretreatment. Sensitization persisted for as long as 2 months after the last injection of cocaine. Cocaine-pretreated mice did not show an increased running response to either morphine or d-amphetamine. The response to cocaine was increased two-fold by treatment with morphine and three-fold by pretreatment with d-amphetamine. Pretreatment with either imipramine or reserpine did not produce sensitization to cocaine. There was no correlation between cocaine sensitization and whole-brain catecholamine levels. There were marked differences in both the running response to cocaine and the extent of cocaine sensitization betwee the parental strains, C57B1/6J and A/J. Experiments with recombinant-inbred lines, derived from C57B1/6By and BALB/cBy mice, suggest that the initial response to cocaine and the development of sensitization are controlled by different genetic determinants.

Animals↗
PubMed1976

Preparation and characterization of two isozymes of choline acetyltransferase from squid head ganglia.

Two isozymes of choline acetyltransferase (Acetyl-CoA:choline O-acetyltransferase, EC 2.3.1.6) have been isolated and purified from squid head ganglia. Each isozyme contains multiple isoelectric forms with isoelectric points ranging from pH 5.0 to 6.2. The isozymes differ in their affinities for cellulose phosphate on column chromatography, as well as in their heat stabilities and in their capacities to be activated by salt. Both isozymes are stabilized by sucrose and by sulfhydryl-protecting reagents such as mercaptoethanol and dithiothreitol.

Acetyltransferases↗
PubMed1976

Preparation and characterization of two isozymes of choline acetyltransferase from squid head ganglia. II. Self-association, molecular weight determinations, and studies with inactivating antisera.

The two isozymes of choline acetyltransferase (Acetyl-CoA:choline O-acetyltransferase, EC 2.3.1.6) from head ganglia of Loligo pealei have been examined by polyacrylamide gel electrophoresis, gel chromatography, and equilibrium sedimentation in the ultracentrifuge. Inactivating antisera, prepared to both native and dithiothreitol-treated isozymes 1 and 2 of squid choline acetyltransferase, were used to demonstrate the immunologic identity of isozymes 1 and 2. Each isozyme appeared to contain two non-identical catalytically active subunits, with molecular weights of approx. 37 000 and 56 000. A staining method was developed to visualize choline acetyltransferase activity in acrylamide gels. The method is based on the formation of a precipitate of manganese ferrocyanide at sites where free coenzyme A is released. By this method, and by analysis of gel slices, it was found that each of the isozymes can form aggregates of several different sizes. The formation of immune precipitates with the aggregates showed the identity of the multiple bands of enzyme protein resolved on disc gel electrophoresis. Isozyme 1 was most active as a small aggregate, whereas isozyme 2 was most active as a large aggregate. Both chromatography on Sephadex G-200 and isoelectric focusing yielded a number of active species with molecular weights ranging from 35 000 to 300 000. In addition, we demonstrated the dissociation of enzyme protein in the presence of 1.0 - 10(-2) M dithiothreitol, the formation of multiple precipitin bands by aged enzyme, and the identity of the different isoelectric fractions of each of the isozymes.

Acetyltransferases↗
PubMed1976

Changes in brain norepinephrine associated with sensitization to d-amphetamine.

Pretreatment of B6AF1/J mice with d-amphetamine HCl 10 mg/kg, twice daily for 5 days, produced a 4-fold increase in the running response to a test dose of 5 mg/kg amphetamine. Amphetamine pretreatment decreased whole-brain norepinephrine levels to 50% of control values and whole-brain dopamine to 85%. The test dose of 5 mg/kg amphetamine lowered whole brain norepinephrine levels of control mice from 0.50 mug/g to 0.28 mug/g in 2 h. In amphetamine-pretreated mice, this injection caused an increase in whole-brain norepinephrine levels from 0.22 mug/g to 0.55 mug/g at 30 min, followed by a decrease to 0.22 mug/g at 60 min. No change in whole brain dopamine levels was observed in either group. Amphetamine sensitization and norepinephrine depletion were still evident 25 days after pretreatment. No cross sensitization to morphine or cocaine was observed. Reserpine pretreatment resulted in a 3-fold increase in locomotor activity following injection of d-amphetamine, 5 mg/kg. No sensitization or changes in catecholamine levels were observed in amphetamine-treated A/J mice. These results suggest that the sensitization produced by amphetamine pretreatment may be related to the depletion of brain norepinephrine.

Animals↗
PubMed1976

Morphine analgesia in mice of different ages.

The analgesic response to 5 mg per kg morphine sulfate was examined in male C57BL/6J mice aged from 2 months to 28 months by the tail-flick assay. The baseline latency of old mice was slightly lower than that of young mice. There was a smaller increase in latency after morphine in old mice than in young mice. Decreased analgesic response in old mice was accompanied by a slower rate of uptake of labeled morphine into the blood after i.p. injection and a longer half-life of the drug. There was no difference between young and old mice in the number of narcotic receptors in the brain.

Aging↗
PubMed1975

A genetic analysis of the response to morphine in mice: analgesia and running.

Two progenitor strains, BALB/cBy and C57BL/6By, their reciprocal F1 hybrids, and seven of their recombinant-inbred derived lines were used to examine the genetic basis of the response to thermal pain, and morphine analgesia at doses of 2.5, 5.0 and 10.0mg/kg. Both the latency of response to thermal pain and the analgesic response differed significantly among the various strains tested. Strong genetic determinants appear to control their responses. Analyses of the data did not permit clarification regarding the linkage of these determinants. Photoelectric activity cages were used to test the running response of the same strains to 12.5, 25 and 40 mg/kg morphine sulfate. The genetic determinants for running activity were different from those for analgesia. There is clear evidence for two or more loci controlling the behavior at 60 and 75 min after injection, but not enough information to define the loci involved.

Analgesia↗
PubMed1975

Perinatal narcotic addiction in mice: sensitization to morphine stimulation.

The injection of morphine sulfate into baby mice twice daily for 5 days increased their running reaponse to morphine when they were tested as adults. If treatment was completed before the mice were )5 days old there was no effect. Sensitization to morphine running was longer-lasting than either analgesic tolerance or tolerance to morphine running may be a form of denervation hypersensitivity that has several features in common with noise-induced sensitization to audiogenic seizures.

Age Factors↗
PubMed1975

Increased running response to morphine in morphine-pretreated mice.

The running response of B6AF1/J mice to 25 mg/kg of morphine sulfate was increased up to 3-fold when this dose was administered either twice daily for 5 days or once a week for 2 or 3 weeks. The effect of weekly pretreatment was proportional to the dose of morphine and lasted as long as 1 month after pretreatment was stopped. There was no sensitization when the mice were less than 15 days old at the time of pretreatment. Of the parental strains, untreated C57Bl/6J mice showed a good running response to morphine, while A/J mice showed little response. Pretreatment of either of these strains produced only slight sensitization. Pretreatment of the hybrids with levorphanol increased the response to morphine. Dextrorphan and naloxone were ineffective. Sensitization by morphine was blocked by naloxone. Increased morphine running was not associated with analgesic tolerance as measured by the tail-flick assay. Morphine pretreatment produced some increase in the running response to amphetamine and to cocaine. Pretreatment with amphetamine or cocaine did not increase the response to morphine.

Aging↗