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Biomedical subjects

A Lajtha

Publications and source records attributed to A Lajtha.

At least 235 records · Page 13Linked to original sources
PubMed1982

Effect of transganglionic degenerative atrophy on opiate receptors in the dorsal horn of the spinal cord.

We investigated alterations in opiate-binding sites in the upper dorsal horn after transection of the related peripheral sensory nerve in rats. The binding of (3H)diprenorphine was measured autoradiographically. The findings indicated a shift of the binding sites, rather than a degenerating disappearance, with a decrease in nerve fibers but an increase in nerve cells. This may be due to latent opiate-binding sites becoming manifest.

Animals↗
PubMed1982

Lithium: effect on [3H]spiperone binding, ionic content, and amino acid levels in the brain of rats.

After prolonged treatment of rats with lithium (pellets, 0.21% lithium carbonate, or 0.5 mg/ml lithium chloride in drinking water) for three months, the level of lithium in plasma was 0.87 meq/liter; in several brain regions, between 1.06-1.39 mueq/g wet weight. The content of sodium and potassium inthe plasma was normal. The level of potassium in the brain regions tested increased by 13-30% and that of sodium by about 10%. Glycine levels increased significantly in all the regions (cerebral cortex, midbrain, cerebellum, and spinal cord). In the cerebellum GABA was also increased, while glutamine was decreased. In midbrain, apart from increases in glycine levels, alanine, valine, GABA and lysine were also increased. In the spinal cord, glutamic acid was also increased. Changes were largely in the putative neurotransmitters. Long-term treatment with lithium also influenced the high-affinity binding of [3H] spiperone in the cerebral cortex and corpus striatum. Two specific binding sites were found in both brain regions; the main change was the reduction in the lower affinity binding site (B max 2).

Amino Acids↗
PubMed1982

Effects of prenatal administration of nicotine on amino acid pools, protein metabolism, and nicotine binding in the brain.

The effects of nicotine on brain protein metabolism and on the properties of the nicotine binding site were investigated in newborn animals exposed to nicotine during gestation. Brain protein synthesis rates measured in vivo were lower by 18% in newborn of treated animals. Protein degradation rates measured in vitro in the presence of nicotine were lower by 13%. The effect was specific for L-(-)nicotine, since D-(+)nicotine, nicotinic acid, or nicotinamide had no effect on degradation rates. Newborn brain amino acid levels, mainly nonessential amino acids and amino acids of putative neurotransmitter function, were changed somewhat; an increase in the level of taurine (13%), threonine (21%), serine (35%) and glycine (35%), and a decrease in lysine (14%) was observed in the offspring of nicotine treated animals (0.5 mg/kg, s.c., 2 x daily throughout gestation). These changes could not account for the decrease in protein metabolism. Nicotine binding was higher by 25% in the offspring of animals exposed to nicotine during gestation. No such increase was found after treatment of adult rats with nicotine, indicating that the properties of the nicotine binding site change with age.

Aging↗
PubMed1982

Changes of neurochemical and electrophysiological indices of rat brain under ethanol intoxication.

It was found that acute ethanol intoxication caused an imbalance of the neurotransmitters in the CNS: accumulation of GABA and serotonin and depletion of catecholamines. Alcohol depression was characterized by suppression of the evoked potentials of the various rat brain structures. Under chronic ethanol intoxication of animals, relative stabilization of the electrophysiological indices of the rat brain activity was observed. This reflects the CNS adaptation to the constant ethanol presence in the blood. This state was also characterized by the relative stabilization of the serotonin system and by the increase of the catecholamine level. Withdrawal of ethanol after prolonged consumption caused accumulation of catecholamines in rat brain, depletion of serotonin and GABA, and increased excitability of the nervous structures. The changes of activity of the GABA- and monoaminergic systems are coupled to manifestation of symptoms of alcohol depression and convulsive reactions during ethanol withdrawal.

Alcohol Withdrawal Delirium↗
PubMed1982

Comparison of the properties of central and peripheral binding sites for cocaine.

Cocaine and its analogs bound saturably to membranes of brain and liver of mice. The binding sites on membranes of liver had a lower affinity for cocaine than those of brain. In addition, there were striking differences between the two tissues in regard to the relative potencies of cocaine analogs in competing with [3H]cocaine for binding. In comparison with the binding sites in brain, those in liver had only moderate stereospecificity, and they discriminated less between the centrally active compounds and the centrally inert analogs.

Animals↗
PubMed1981

Strain differences in opiate receptors in mouse brain.

Various opiate ligands were bound to brain membranes of mice of the Recombinant Inbred System. The specific binding of low levels of [3H]naloxone, [3H]dihydromorphine and [3H]ethylketocyclazocine was disturbed in a similar fashion among the inbred strains, and in a pattern different from that observed for [3H](D-Ala2,D-Leu5)-enkephalin. The results indicate that the inbred strains differ in mu- and delta-type binding and support the concept of multiple opiate receptors in mouse brain.

Animals↗
PubMed1981

Drug-induced changes in the composition of the cerebral free amino acid pool.

The effects of insulin, hydroxybutyrate, deoxypyridoxine, chlorpromazine, codeine, morphine, puromycin, and cycloheximide on the composition of the free amino acids in mouse and rat brain were tested. Significant changes occurred in a number of amino acids with most compounds tested; the largest was of alanine (a 50% increase with glucose, a 50% decrease with drugs); histidine was often increased, and the nonessential amino acids were mostly decreased. The pattern of changes was somewhat different in the mouse brain from that in the rat brain. Changes of amino acid levels may participate in the pharmacological action of a number of compounds.

Amino Acids↗
PubMed1981

Effect of lithium and sodium ions on opiate- and dopamine-receptor binding.

The effects of lithium and sodium were studied in the corpus striatum and cerebral cortex of rats. Lithium was inhibitory at low concentrations but at 20 mM it increased the binding of [G-3H]naloxone (specific activity 15.6 Ci/mmol). Sodium stimulated the high-affinity binding of this compound. Membranes obtained from the rats treated with lithium showed lower specific binding of both [3H]naloxone and [3H]DHM. Binding of [3H]d-alanine Leu-enkephalin was not changed in the brains of lithium-treated rats, but that of [3H]-spiroperidol was lowered. Cerebral cortex and striatum of lithium-treated rats had a decreased apparent dissociation constant and a lower receptor concentration of naloxone binding sites.

Animals↗
PubMed1981

Elevation of cerebral levels of nonessential amino acids in vivo by administration of large doses.

Taurine, aspartic acid, glutamic acid, glycine, and GABA were administered either intragastrically or in liquid diets to mice and rats. This resulted in a great increase in the plasma concentration of the administered amino acid, with plasma levels remaining elevated for several days. The prolonged increase in plasma levels resulted in significant increases in brain levels. Under these experimental conditions, taurine, aspartic acid, and glutamic acid were increased 30-60%; glycine and GABA 100%. During these experiments, plasma levels of taurine, aspartate, and glutamate were below brain levels; those of glycine and GABA were above. The findings show that even slowly penetrating amino acid levels can be increased in brain after parenteral administration of large doses.

Amino Acids↗
PubMed1981

The effect of naloxone on enkephalin catabolism.

Naloxone strongly inhibited the breakdown of Met- and Leu-enkephalin when the substrate was incubated with brain homogenate, supernatant, or partially purified soluble aminopeptidase, but it had no effect on the mitochondrial fraction. Arylamidase was also inhibited by naloxone. The inhibitory effect of naloxone on the soluble aminopeptidase was in a linear relationship with concentration in the range of 8-500 microM. The KI for Met-enkephalin is 0.6 mM and for Leu-enkephalin is 2.0 mM. When the naloxone was administered intraperitoneally to the mice, its effects were somewhat different from its effects in vitro. It inhibited the brain catabolism of Met-enkephalin but not of Leu-enkephalin or Tyr-beta NA in vitro. In vivo, acute morphine in mice decreased the Met-enkephalin hydrolysis but increased the Leu-enkephalin hydrolysis. Chronic morphine (by morphine pellet implantation) increased the breakdown rate of enkephalin and of Tyr-beta NA. Naloxone (1 mg/kg) could not reverse the effects of morphine, although abstinence syndrome and stereotypical jumping were precipitated. Naloxone decreased the Leu-enkephalin level in the control mice but did not affect it in the addicted mice.

Aminopeptidases↗
PubMed1981

Brain slice protein degradation and development.

Protein degradation rates were measured in brain slices prepared from rats of various ages. This was done by adding the protein synthesis rate, determined by incorporation of a labeled precursor, and the net protein degradation rate, determined by measuring the changes with time of total free amino acids. These rates are about 30% higher than those previously calculated from data on protein synthesis rates and protein accumulation rates in vivo. The protein degradation rates in brain slices diminish with age; i.e., 2-day cerebellum greater than 2-day cerebral hemisphere greater than 12-day cerebral hemisphere greater than young adult cerebral hemisphere. Protein degradation rates in slices from young brain are initially slightly higher than protein synthesis rates, resulting in a small net degradation with time. Unlike slices from adult brain, the protein degradation rates in slices from young brain decline only modestly with time for as much as 100 min of incubation. The characteristics of protein degradation in brain slices from young animals are roughly similar to some of the data calculated for protein degradation in vivo, suggesting that this system may prove useful for studying factors which control or affect brain protein degradation.

Age Factors↗
PubMed1981

Noncholinergic, saturable binding of (+/-)-[3H]nicotine to mouse brain.

(+/-)-[3H]Nicotine was bound saturably to crude particulate, and synaptosomal-mitochondrial fraction from mouse brain. Scatchard and Hill plots of the binding data are in agreement with the existence of two independent classes of binding sites with high (Kd of 0.1-0.4 microM) and low(Kd is 20 microM) affinities, although negative cooperativity or a two-step model of ligand-receptor interaction cannot be ruled out. Nicotinic or muscarinic agonists and antagonists had little or no affinity for the nicotine binding sites, suggesting that nicotine binds in brain to noncholinergic sites. The binding did not display stereospecificity; this is consistent with the similarity in the pharmacological effects of (-)- and (+)-nicotine. Our results indicate that binding studies with [3H]nicotine should be interpreted with extreme caution.

Animals↗
PubMed1981

Binding of [3H]cocaine in mouse brain: kinetics and saturability.

Kinetic experiments indicate that association of [3H]-cocaine to its binding site in brain occurs rapidly (seconds). Dissociation of membrane-bound cocaine is also rapid, with a dissociation half-life in seconds; this raises the question of whether membrane-bound cocaine is released during the time required for rapid filtration of tissue-containing filters. Results from experiments with increasing numbers of filter-washes indicate that there is no significant loss of [3H]-cocaine saturably bound to brain membranes within the time-scale of the rapid filtration procedure. In addition, saturation analysis of binding data obtained with the filtration procedure and with the centrifugation method give similar estimates of the affinity (dissociation constant: 0.8 microM) and the maximal binding (5 pmol/mg of protein) of cocaine. However, the nonspecific binding and the experimental error in the saturable binding are considerably greater in centrifugation assays than in filtration assays.

Animals↗
PubMed1981

Attempts at induction of phenylalanine hydroxylase in thermophilic bacteria and induction of thermophily in mesophiles.

Some moderate and extreme thermophilic bacteria grew well on media other than the recommended basic media. Attempts to induce phenylalanine hydroxylase (Phe H) in the various thermophiles as well as mild thermophily in the mesophiles Pseudomonas sp ATCC 11299a and Chromobacterium violaceum ATCC 12540 were unsuccessful. Evidence is presented indicating that the enzyme in the latter two organisms may be membrane bound. The level of Phe H activity induced was not always consistent with the level of the inducer phenylalanine (Phe) in the growth medium.

Bacteria↗