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Biomedical subjects

L M Kopeloff

Publications and source records attributed to L M Kopeloff.

At least 19 recordsLinked to original sources
PubMed1985

Convulsive thresholds in mice: action of 6-hydroxydopamine and eboracin.

The neurotoxin, 6-hydroxydopamine, when injected intraperitoneally, protected mice from seizures induced by pentylenetetrazol (Metrazol) and altered the nature of the convulsive response induced by an auditory stimulus. Conversely, the indenopyrrole, eboracin, protected mice from seizures induced by auditory stimulation and altered the response to Metrazol. In each case the altered response was characterized by a marked prolongation of the clonic component without progression to the generalized tonic phase. It appeared, therefore, that 6-hydroxydopamine raised the threshold to tonus in audiogenic seizures, and eboracin raised it in Metrazol seizures. Eboracin raised threshold to clonic phase in audiogenic seizures whereas 6-hydroxydopamine raised it in Metrazol seizures. Our findings showed that in Metrazol and audiogenic seizures thresholds to clonus and progression to the tonic phase were mediated by different biochemical mechanisms and suggested that agents controlling induction of clonic manifestations in one seizure model may be those involved in controlling seizure spread in the other.

Acoustic Stimulation↗
PubMed1985

Comparison of anticonvulsive properties of eboracin and phenytoin in mice.

The in vivo effects of phenytoin (diphenylhydantoin, Dilantin) and the experimental anticonvulsant, eboracin, a substituted indenopyrrole, were compared in mice. Pretreatment with varying dosages of either agent followed by challenge with the chemoconvulsant pentylenetetrazol (Metrazol) indicated that eboracin provided slightly less protection against seizures than phenytoin and was much less toxic. Intermediate doses of either agent led to a form of clonic status epilepticus which persisted for an average of 18 min in phenytoin-treated and 58 min in eboracin-treated mice. Pretreatment with higher or lower doses did not lead to these manifestations. Animals in which this syndrome had been induced should be of value in studies of the chemistry and physiology of the clonic state.

Animals↗
PubMed1982

Eboracin: a substituted indenopyrrole active against metrazol-induced, audiogenic and electroshock seizures in mice.

1. Pretreatment with eboracin, a methyl ester of a trioxyindenopyrrole, inhibited the tonic phase of pentylenetetrazol (Metrazol)-induced, audiogenic and electroshock seizures in mice. 2. In animals challenged with Metrazol a dose of 28 mg/kg eboracin prevented 50% of tonic-clonic responses. 3. In animals exposed to electroshock or auditory stimulation the dose required to produce a 50% reduction in tonic-clonic seizures was 30 mg/kg and 35 mg/kg, respectively. 4. The 50% lethal dose was 832 mg/kg, indicative of eboracin's relatively low toxicity and high therapeutic index. 5. Pretreatment with eboracin led to a prolongation of the myoclonic phase of Metrazol seizures, similar to that observed after phenytoin.

Acoustic Stimulation↗
PubMed1982

Effect of eboracin on convulsive seizures in mice: enhancement of myoclonus and inhibition of the tonic phase.

Eboracin, a substituted trioxyindenopyrrole, inhibited the tonic component of convulsive seizures induced in mice by pentylenetetrazol, electroshock or auditory stimulation. Single doses decreased the incidence of tonic-clonic seizures (ED50=28-35 mg/kg); complete inhibition of tonus followed doses of 40-150 mg/kg. A dose of 75-150 mg/kg of eboracin prolonged the duration and increased the severity of the myoclonic component of seizures induced by pentylenetetrazol.

Acoustic Stimulation↗
PubMed1980

Serotonin and norepinephrine: long-term decrease in rate of synthesis in brain of rats primed with p-chlorophenylalanine.

Rats which had been primed with the serotonin depletor, p-chlorophenylalanine, and sacrificed months later were found to have the same resting levels of brain serotonin and norepinephrine as unprimed controls. However, when treated with the monoamine oxidase inhibitor, tranylcypromine, the former showed a significantly lower accumulation of these biogenic amines than their tranylcypromine-treated unprimed counterparts. These findings indicate that brain serotonin, which had been lowered at the outset by p-chlorophenylalanine, had returned to normal levels but that the priming procedure might have resulted in a long-term decrease in the turnover rates of serotonin as well as norepinephrine. Primed animals may prove suitable as models of disturbed biogenic amine metabolism with possible relevance to schizophrenia and other brain dysfunctions.

Animals↗
PubMed1980

Post-ictal resistance to audiogenic seizures in inbred mice.

Inbred audiosensitive mice exposed to a prolonged auditory signal recovered and remained refractory to further audiogenic seizures as long as the signal was continued. Susceptibility to audiogenic seizures returned upon cessation of sound. The rate of return was the same whether the sound stimulus was brief or prolonged. In a small proportion of test animals, which failed to become fully refractory, the continuing auditory stimulus proved lethal. Mice maintained in the post-seizure refractory state were fully susceptible to Metrazol-induced seizures.

Acoustic Stimulation↗
PubMed1978

Anticonvulsive effect of p-chlorophenylalanine in mice on a low magnesium diet.

We have reported previously that para-chlorophenylalanine prevented seizure manifestations in an inbred strain of mice genetically predisposed to audiogenic seizures. We now find that this protective effect is not limited to a particular inbred strain of susceptible animals but can be demonstrated in Swiss-Webster and CF No.1 strains which were not originally subject to audiogenic seizures but in which we have induced audiosusceptibility through maintenance on a low magnesium diet.

Acoustic Stimulation↗
PubMed1976

Audiogenic seizures in mice: influence of agents affecting brain serotonin.

Brain serotonin levels and susceptibility to audiogenic seizures were examined in a strain of inbred audiosusceptible mice and in control mice at intervals from two hours to one week after treatment with several agents known to modify serotonin metabolism. Although p-chlorophenylalanine produced a gradual decrease in brain serotonin there appeared to be no temporal correlation between this effect and the rapid reduction in seizure susceptibility. 5-Hydroxytryptophan and tranylcypromine led to significant increases in serotonin, but only the former caused a proportinal reduction in seizure activity. Reserpine and alpha-propyldopacetamide decreased serotonin levels but only reserpine caused an intensification of seizure activity proportional to serotonin changes. On the basis of our data, effects of 5-hydroxytryptophan and reserpine on seizure susceptibility appear to be linked to observed brain serotonin levels; further studies are needed to elucidate the mode of action of p-chlorophenylalanine.

5-Hydroxytryptophan↗
PubMed1976

Additive effect of 5-hydroxytryptophan and p-chloro-phenylalanine in preventing audiogenic seizures in inbred mice.

Convulsive responsiveness of O'Grady mice, inbred for susceptibility to audiogenic seizures, was decreased following treatment with the serotonin precursor, 5-hydroxytryptophan, or serotonin depletor, p-chlorophenylalanine. Neither agent exerted any antagonistic or synergistic action on the effect of the other. Upon sequential administration, their effects were additive. There was no indication that the increase in brain serotonin due to administration of its direct precursor interfered with the protective effect of p-chlorophenylalanine against seizures. Neither was there evidence that p-chlorophenylalanine-induced interruption of biosynthesis which led to severe depletion of brain serotonin affected the protective action of 5-hydroxytryptophan.

5-Hydroxytryptophan↗
PubMed1976

Recurrent immunogenic interstitial keratitis. Production in the guinea pig by extraocular means.

Combinations of intracutaneous (IC) and intravenous (IV) injections of bovine gamma-globulin (BGG) or bovine serum albumin (BSA) induced interstitial keratitis in 24 of 29 guinea pigs. For IC injection, antigen was incorporated in complete Freund adjuvant. When IC and IV BGG reactants were administered simultaneously, corneal opacities appeared after 11 to 19 days and persisted for periods of 2 to 11 days. Following a free interval, a secondary reaction of somewhat shorter duration occurred. A BGG-adjuvant emulsion administered three or five weeks after IV injection of BGG induced an accelerated and intensified response followed by a protracted course of recurring corneal opacities. Irritative brain lesions produced by implanted alumina cream or cobalt powder prior to simultaneous IC and IV antigenic treatment were associated with diminished conreal reactions (alumina) and a number of tertiary eye responses.

Aluminum↗