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Biomedical subjects

E D Levin

Publications and source records attributed to E D Levin.

At least 127 records · Page 7Linked to original sources
PubMed1988

[Primary structure of intracellular serine proteinase from Bacillus amyloliquefaciens. I. Isolation of the enzyme and amino acid sequence of peptides of tryptic hydrolysate].

Method of isolation of intracellular serine protease was modified. Gramicidin S-sepharose CL-4B with a higher content of the ligand, synthesized through a modified procedure, was used as an affinity sorbent which simplified the purification and led to the pure enzyme with high specific activity and 90% yield. Trypsin hydrolyzate of the protease was separated by ion-exchange chromatography on a sulphocationite resin followed by paper chromatography and paper electrophoresis to yield twenty-five individual peptides. Their complete or partial sequences, corresponding in total to 146 amino acid residues, were determined by the manual Edman procedure.

Amino Acid Sequence↗
PubMed1987

Neuroleptic-induced oral movements in rats: methodological issues.

In three separate experiments groups of rats were chronically administered neuroleptics in a variety of ways (chronic injections, subcutaneous implants, and decanoate injections) and examined for oral movements (OMs) in two different tests: in an open cage using a human observer, or in a plexiglas tube enclosure, where OMs were monitored both by a human observer and computerized video analysis system. These two testing methods showed different effects of neuroleptic administration. In the open cage, OMs tended to be enhanced during chronic neuroleptic exposure and to rapidly subside upon drug withdrawal. The enhanced OMs were especially present just after drug injections, when activity levels were low. In the observation tube environment, however, OMs tended to be low soon after drug treatments, and elevated upon withdrawal. Thus, the type of behavioral test used determines how neuroleptic-induced increases in oral activity should be interpreted.

Animals↗
PubMed1987

Characterization of the analgesic effects of the benzodiazepine antagonist, Ro 15-1788.

Three experiments were carried out in rats to evaluate the analgesic effects of the benzodiazepine antagonist, Ro 15-1788. Expt. 1 demonstrated a diazepam reversible analgesic effect of Ro 15-1788 using the tail-flick test. Expt. 2 analyzed the effects of Ro 15-1788 in the hot-plate test at various doses. Low doses of Ro 15-1788 proved analgesia 20 min after drug injection, whereas high doses had no analgesic effect on the 20 min test, but were effective on the 50 min test. Expt. 3 demonstrated that the opiate antagonist, naloxone, had no effect on analgesia produced by Ro 15-1788 in the hot-plate test. The analgesic effects of Ro 15-1788 may be attributable to its reported anxiogenic properties.

Analgesics↗
PubMed1987

Psychopharmacological investigations of a lead-induced long-term cognitive deficit in monkeys.

This study investigated pharmacological manipulations of the cholinergic (ACh) and dopaminergic (DA) transmitter systems in monkeys with a long-term lead-induced cognitive deficit on delayed spatial alternation (DSA). Both ACh and DA have been found to be affected by developmental lead exposure and to be involved with performance on spatial learning and memory tasks. The lead-induced deficit in performance accuracy on DSA persisted throughout the 2 years of this experiment, which ended more than 8 years after the end of the postnatal lead exposure. Acute administration of agonists and antagonists of the ACh and DA systems did not elicit differential effects from the lead-exposed and control groups in terms of DSA per cent correct performance. The ACh antagonist, scopolamine, caused a dose-related decline in performance in both groups. Significant amelioration of the lead-induced DSA deficit was achieved by chronic treatment with the DA agonist, L-dopa. After withdrawal from L-dopa, the lead-related deficit reappeared. Improvement in performance of the lead-treated group was also seen after chronic amphetamine administration, but this effect was not significant. These data implicate DA mechanisms in the long-lasting cognitive effects of developmental lead exposure. The alleviation of the deficit with chronic administration of a DA precursor points to a possible line of treatment for the cognitive effects of developmental lead exposure.

Acetylcholine↗
PubMed1987

Neurobehavioral effects of chronic halothane exposure during developmental and juvenile periods in the rat.

Chronic exposure of rats to the surgical anesthetic agent halothane during development has been found to cause both neural and behavioral impairment. Among the halothane-induced deficits are retarded synaptogenesis and impaired spontaneous alternation. It is unclear how long after birth the susceptibility to the neurotoxic effects of halothane persists. The present study compared in rats the effects of halothane exposure on synaptic density and spontaneous alternation during early and late periods of maturation. All three experimental groups were exposed to 100 parts per million of halothane for 8 h/day, 5 days/week. One group (early exposure) was exposed from day 2 of conception until 30 days after birth. The second group (late exposure) was exposed to the same amounts from day 31 until day 90 after birth. The third group (continued exposure) received both periods. The control group was treated in the same way, but was not exposed to halothane. As found in the previous study, there were greater effects of halothane on synaptogenesis than on spontaneous alternation; impairment of spontaneous alternation behavior was found only with the early exposure. Deficits in synaptic density were found with both early and late exposure, although the early exposure had more severe effects. Halting the exposure to halothane on day 30 reinstated control-like rates of synaptogenesis, but the deficit in synaptic density from the early exposure persisted into adulthood. The potent neurotoxic effect of halothane in suppressing synaptogenesis highlights not only its potential as a hazard but also its potential as an experimental tool for manipulating the rate of synaptogenesis and examining the relationship between synaptic development and behavioral maturation.

Aging↗
PubMed1987

Chronic nicotine and withdrawal effects on body weight and food and water consumption in female rats.

Female rats were used to examine the effects of chronic nicotine administration and withdrawal on food and water consumption and body weight. Rats with chronic nicotine pellet implants consumed significantly less food and water than controls for the first five days and then gradually returned to control levels of consumption. The lowest level of body weight was reached on day 9 after which there was a slow return to control weights by day 21. When the nicotine pellets were removed from the short-term exposure group on day 14, they showed significant hyperphagia and hyperdipsia and a very rapid weight gain for the next several days, which clearly outpaced the recovery of weight in the long-term nicotine exposure group. These results show that in female rats changes in weight during chronic nicotine administration and withdrawal are accompanied by changes in rates of consumption. In addition, nicotine withdrawal can cause hyperphagia and hyperdipsia even though levels of consumption had previously returned to control levels and even though the route of nicotine administration was not oral.

Animals↗
PubMed1987

Chronic haloperidol effects on oral movements and radial-arm maze performance in rats.

Rats were examined for the development of adverse motor and cognitive effects during and after 24 weeks of chronic haloperidol (HAL) administration using an 8-arm maze and a computerized apparatus for measuring spontaneous oral movements. In the maze, HAL caused a significant decline in choice accuracy only during the first week of administration, whereas it caused a significant decline in locomotor speed throughout drug administration. There were no effects of HAL on maze behavior after withdrawal. Haloperidol reduced the number of mouth movements during drug administration, but after withdrawal there was a significant increase. This replicated a previous finding from our lab. The oral movements which did occur in the HAL-treated rats were slower than normal. The timing of the HAL-induced cognitive dysfunction was similar to the Parkinson-like disorder shown by patients given chronic neuroleptics, whereas the timing of the increase in oral movements after the withdrawal of HAL was more related to the appearance of tardive dyskinesia. There was evidence in both tests of a persisting sedation during chronic neuroleptic administration.

Animals↗
PubMed1987

Effects of the nicotinic receptor blocker mecamylamine on radial-arm maze performance in rats.

Lesions of cholinergic neurons have been found by many investigators to impair choice accuracy in the radial arm maze. Because muscarinic receptor blockers, such as scopolamine, have also repeatedly been found to impair choice accuracy in the radial-arm maze, it has generally been thought that the critical effect of cholinergic lesions is the deafferentation of muscarinic receptors. The possible involvement of nicotinic receptors in the cholinergic bases of cognitive performance in the radial-arm maze has not been as well investigated. The present study examined the effects of the blockade of nicotinic receptors on performance of female Sprague-Dawley rats in the radial-arm maze. Acute administration of the the nicotinic receptor blocker, mecamylamine (10 mg/kg) was found to significantly impair radial-arm maze choice accuracy. This dose also caused a significant increase in response latency in the maze. The effect on choice behavior but not locomotor speed seemed to be due to the central effects of mecamylamine, because administration of the peripheral nicotine receptor blocker, hexamethonium (20 mg/kg), did not impair choice accuracy, even though it did increase response latency to a similar degree as the 10-mg/kg dose of mecamylamine. Lower doses of mecamylamine (2.5 and 5 mg/kg) did not impair choice accuracy. These results indicate that central nicotinic as well as muscarinic cholinergic receptors are involved with cognitive functioning.

Animals↗
PubMed1986

Effects of the dopamine D-2 receptor agonist, LY 171555, on radial arm maze performance in rats.

Rats trained to run through an 8-arm radial maze for food reinforcement were injected with a broad range of doses of the dopamine D-2 receptor agonist, LY 171555. Deficits were detected by the choice measures of entries to repeat and arms entered in the first eight choices. There was a dose-related increase in latency to finish the maze even though there was no significant increase in the number of choices needed to finish the maze.

Animals↗
PubMed1986

Scopolamine effects on Hamilton search task performance in monkeys.

The Hamilton search task, a test of spatial memory, was given to adult monkeys after administration of scopolamine. Three monkeys had been exposed to lead during development and two were controls. The task consisted of opening eight boxes, one per trial, for food reinforcement, with a 20 second delay between trials. The monkey had to remember which boxes it had already opened and avoid them to obtain the remaining reinforcements. Percent correct response, openings-to-repeat, trials per session, repetitive index and response latency were measured. There were no significant lead-related effects. Significant scopolamine-induced deficits were detected with four of the measures. The low doses of scopolamine (1-3 micrograms/kg) did not affect response accuracy, but 15 and 30 micrograms/kg caused impairments. Only 30 micrograms/kg substantially increased latency. This is like other memory tests in monkeys and rats in that it is sensitive to anticholinergic challenge. Cognitive performance deficits were detected at a dose (15 micrograms/kg) which did not cause increased response latency. The Hamilton search task is a flexible and sensitive memory task for monkeys, analogous to the radial arm maze in the rat.

Animals↗
PubMed1986

Behavioral effects of chronic exposure to low concentrations of halothane during development in rats.

Long-term behavioral effects of chronic exposure to low concentrations of halothane were evaluated in rats exposed to low (12.5 ppm) concentrations from day 2 of conception until either 30 (halothane-30) or 60 (halothane-60) days after birth. Rats similarly treated but not exposed to halothane served as controls. When these rats were tested for radial arm maze exploration as adults (1 yr old) both exposure groups showed significant deficits compared with controls. The halothane-treated rats entered significantly fewer arms before reentering an arm (entries-to-repeat). At 55 days of age, in the spontaneous alternation test, response speed was significantly slower than controls in both halothane-30 and halothane-60 rats. This effect was not seen in rats more than 55 days old. Replicating previous results, the halothane-60 rats showed deficits in learning a light-dark discrimination. This deficit was not seen with halothane-30 rats, indicating that continued halothane exposure during the 30- through 60-day period was necessary for inducing a noticeable long-term learning deficit. The results show that chronic exposure of rats to low concentrations of halothane during development results in subsequent behavioral alteration, and that termination of halothane exposure at 30 days of age rather than at 60 days of age avoids some of the signs of behavioral impairment.

Analysis of Variance↗
PubMed1985

Effects of halothane on the development of rat brain: a golgi study of dendritic growth.

Dendritic growth was studied in rats exposed to halothane in utero for the entire gestation period and 60 days after birth. The exposure conditions were control, intermittent halothane (25 +/- 5 ppm or 100 +/- 5 ppm, 8 h/day, 5 days/week), or continuous halothane (25 +/- 5 ppm, 24 h/day, 7 days/week). Dendritic growth in terms of branch numbers and length was most advanced in the control groups, followed by those groups exposed to 25 +/- 5 ppm halothane intermittently, 25 +/- 5 ppm halothane continuously, and 100 +/- 5 ppm halothane intermittently. The latter two exposure conditions exerted identical effects on dendritic growth. The order of this dendritic growth level established at 5 postnatal days remained the same throughout the first 95 postnatal days in both the entorhinal cortex and subiculum. The effect of halothane on dendritic growth appeared to be enduring, and the delay in the initial dendritic growth caused by halothane was not compensated for by an increased rate of dendritic growth.

Animals↗
PubMed1985

Effects of halothane on synaptogenesis and learning behavior in rats.

Synaptic density was quantitated in the entorhinal cortex and subiculum of rats at 5, 21, 34, and 95 postnatal days. These rats were offspring of mothers that had been subjected to four different concentrations of halothane during gestation and for 60 days after birth. The exposure conditions were control, intermittent halothane (25 +/- 5 ppm or 100 +/- 5 ppm, 8 h/day, 5 days/week) and continuous halothane (25 +/- 5 ppm, 24 h/day, 7 days/week). Synaptic density in rats exposed to halothane was significantly less than in control rats. Animals exposed intermittently to 25 +/- 5 ppm halothane had higher synaptic density than animals exposed continuously to 25 +/- 5 ppm halothane or intermittently to 100 +/- 5 ppm halothane. The latter two exposure conditions exerted similar effects. The lag in synaptic development was established at 5 days postnatal and remained the same throughout the first 95 postnatal days in both the entorhinal cortex and subiculum. Delayed synaptogenesis caused by halothane was indicated by the presence of growth cones in halothane-exposed rats to 34 days compared with 21 days in the control rats. The spontaneous alternation test indicated that the delayed synaptogenesis by halothane was sufficient to suppress behavioral development. Thus, the delay in the initial synaptic maturation caused by halothane exposure in utero may result in permanent morphologic and functional deficits of the brain.

Aging↗
PubMed1982

[Differences in primary structures of delta-endotoxins produced by various serotypes of Bacillus thuringiensis].

The primary structures of delta-endotoxins (crystal-forming proteins) produced by two serotypes of Bacillus thuringiensis--V (var. galleriae) and III (var. alesti) were compared. These proteins differ by the specificity of their action on Lepidoptera larvae as well as by their molecular weights. To evaluate the homology of primary structures the tryptic hydrolysates of both endotoxins were fractionated by ion-exchange and thin-layer cellulose chromatography with a subsequent amino acid determination in the hydrolysates of thus obtained the fraction. Only 10%, of the fractions gained from the tryptic hydrolysates of the two delta-endotoxins had similar amino acid composition. In control experiments on comparison of two hydrolysates of the same delta-endotoxins the percentage of fractions with similar amino acid composition was as high as 50%, which reflects the tendency of this approach to overestimate the extent of the differences between the two sequences. Hence the delta-endotoxins produced by two serotypes of Bacillus thuringiensis, being clearly homologous, reveal substantial differences in their amino acid sequences, which are dispersed along the whole polypeptide chain. These striking differences in the primary structures are indicative of an unusually high rate of their evolution, which may be of functional importance for B. thuringiensis serotypes adaptation to different ecological niches.

Amino Acid Sequence↗
PubMedDate not supplied

Effects of nicotinic dimethylaminoethyl esters on working memory performance of rats in the radial-arm maze.

Nicotine has been found to improve memory performance in a variety of tests, including the radial-arm maze. This improvement, together with the consistent finding of a decline in cortical nicotinic receptor concentration in Alzheimer's patients, has fueled the search for novel nicotinic ligands with therapeutic potential. In the current studies, a series of nicotinic compounds was tested for effects on working memory performance in the radial-arm maze. One of the three compounds tested, DMAE II (dimethylaminoethanol cyclohexyl carboxylate fumurate), produced significant improvements in working memory performance. In the first experiment, this drug produced a biphasic dose-response curve with improved performance at the 20-mg/kg dose but not at 10 or 40 mg/kg. In a second round of DMAE II administration, the same rats showed a significant improvement with the 40-mg/kg dose. In the second experiment, a new set of rats also showed a biphasic dose-response to DMAE II. The 20-mg/kg dose caused a significant improvement whereas the 40-mg/kg dose did not. Interactions of DMAE II with nicotine and mecamylamine were also studied. Nicotine (0.2 mg/kg) by itself caused a significant improvement in working memory performance. No additive effects of DMAE II with nicotine were seen. In fact, some attenuation of response was seen with the combination. Choice accuracy data for mecamylamine could not be analyzed because of excessive sedation and nonresponding. These studies show that, like nicotine, the nicotinic ligand DMAE II causes an improvement in radial-arm mace choice accuracy. The lack of additivity with nicotine may have been to the partial agonist effects of DMAE II.

Animals↗