Lysergic acid diethylamide: radioimmunoassay

A radioimmnunoassay for d-lysergic acid diethylamide (LSD) is described. Antibodies to LSD were obtained by immunizing rabbits with a conjugate of LSD and human serum albumin. The specificity of the antibody was shown by competitive binding studies. The method has been used to detect the presence of LSD in human urines. Picogram amounts can be measured by this assay.     

Lysergic acid diethylamide: effect on embryos

Injection of lysergic acid diethylamide tartrate into mice in early pregnancy caused a 57 percent incidence of grossly abnormal embryos.     

Lysergic acid diethylamide and stimulus generalization: rate-dependent effects

A stimulus generalization procedure was used to investigate the effects of LSD on sensitivity to auditory stimuli in rats. The shape of the generalization gradient was changed after administration of the drug only with a dose which produced decreases in relatively high rates of responding.     

Lysergic acid diethylamide: effects on the developing mouse lens

High doses (5 x 10-(6) gram) of LSD-25 given to Swiss-Webster females on gestation days 6, 7, 8, or 9 caused a high incidence of anterior subcapsular lens abnormalities. Accompanying this, the lens epithelium was often hyperplastic, and the lens bow was widened posteriorly in a fashion similar to cataracts induced by x-radiation. Confirmation of this effect of LSD-25 was obtained by a (duplicate) experiment 1 year after the observations reported.     

Lysergic acid diethylamide: sensitive neuronal units in the midbrain raphe

Units in areas of the midbrain rich in neurons containing serotonin respond to parenteral injections of d-lysergic acid diethylamide by a reversible cessation of spontaneous activity. The dose required is at or below threshold for gross behavioral effects. An inhibition of neurons containing serotonin after administration of d-lysergic acid diethylamide could account for the decreased metabolism of serotonin produced by this drug.     

Lysergic acid diethylamide: role in conversion of plasma tryptophan to brain serotonin (5-hydroxytryptamine)

Injections of D-lysergic acid diethylamide decrease the turnover rate of 5-hydroxytryptamine of rat brain, as measured from the conversion of (14)C-tryptophan into (14)C-5-hydroxytryptamine. The 2-bromolysergic acid diethylamide given in doses fivefold greater than those of lysergic acid diethylamide fails to change the rate of (14)C-tryptophan conversion into (14)C-5-hydroxytryptamine. The effect of D-lysergic acid diethylamide is discussed with regard to its action on brain serotonergic neurons and its psychotomimetic effects.     

Lysergic acid diethylamine: mutagenic effects in Drosophila

d-Lysergic acid diethylamide causes a significant increase in recessive lethal mutations in the X chromosome of Drosophila males after intraperitoneal injection of massive doses.     

Apomorphine: modification of its hyperthermic effect in rabbits by p-chlorophenylalanine

The hyperthermic response of rabbits to apomorphine, a dopaminergic agonist, is abolished by prior treatment with p-chlorophenylalanine. If such 5-hydroxytryptamine (5-HT)-depleted animals are administered a peripherally acting decarboxylase inhibitor plus 5-hydroxytryptophan, central stores of 5-HT are regenerated and the hyperthermic response to apomorphine is restored in part. The effects of apomorphine in rabbits with elevated concentrations of 5-HT are not different from those in control animals. The behavioral effects of apomnorphine appear to be constant in all groups of animals tested. It is suggested that the hyperthermic effects of apomorphine in rabbits require the presence of 5-HT.     

Congenital malformations induced by mescaline, lysergic acid diethylamide, and bromolysergic acid in the hamster

Malformations of the brain, spinal cord, liver, and other viscera; body edema; and localized hemorrhages were found in fetal hamsters from mothers injected subcutaneously with a single dose of mescaline, lysergic acid diethylamide, or 2-bromo-D lysergic acid diethylamide on the 8th day of pregnancy. In addition, all three drugs produced an increase in the percentages of small fetuses per litter, of resorptions, and of fetal mortality.     

A quantifiable behavioral correlate of psychotogen and tranquilizer actions

A representative psychotogen, lysergic acid diethylamide (LSD-25), in doses small enough to be devoid of gross effects, increases response latency in rats to a tone indicating the availability of water reward; this effect is greatly reduced by prophylactic administration of a representative phenothiazine tranquilizer, chlorpromazine (CPZ), in doses that per se do not affect performance. The nature of the chlorpromazine action and its competition with lysergic acid diethylamide is revealed by the effects of chlorpromazine in larger doses.     

Leukocytes of humans exposed to lysergic acid diethylamide: lack of chromosomal damage

Leukocyte cultures from eight human subjects who had had recent exposure to large doses of lysergic acid diethylamide were examined for chromosome abnormalities. The number of abnormalities was not significantly greater than that in control cultures.     

Chromosomal effect in vivo of exposure to lysergic acid diethylamide

Chromosome studies of persons exposed to lysergic acid diethylamide, either self-administered or received during medical therapy, failed to demonstrate significant chromosomal damage.     

( 3 H)lysergic acid diethylamide: cellular autoradiographic localization in rat brain

Intravenous administration of [(3)H]lysergic acid diethylamide(LSD) to rats resulted in accumulation of the drug in the brain within 15 minutes. Autoradiographic methods were used to differentiate free and bound [(3)H]LSD in brain tissue.Free [(3)H]LSD was generally distributed in the pituitary and pineal glands, cerebellum, hippocampus,and choroid plexus.Bound [(3)H]LSD was localized in neurons of the cortex, caudate nucleus, midbrain, and medulla,as well as in choroid plexus epithelium.