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PubMed1996

Development of a stand-alone affinity clean-up for lysergic acid diethylamide in urine.

A total analysis scheme for lysergic acid diethylamide (LSD) from human urine is described. A simple ELISA technique led to the development and optimization of an affinity clean-up cartridge, resulting in high purification factors with a single combined extraction/clean-up step. LSD can be measured with a straightforward HPLC-fluorescence technique, which minimizes operating complexity and process implementation time. The method has been applied to urine containing 0.5 ng ml-1 LDS, and the ability of high-affinity materials to preconcentrate a sample into a small volume should allow the working range of the procedure to be adjusted as required.

Chromatography, Affinity↗
PubMed1977

Lysergic acid diethylamide: evidence for stimulation of pituitary dopamine receptors.

Lysergic acid diethylamide (LSD), 0.05 mg/kg and 0.20 mg/kg, significantly decreased plasma prolactin (PRL) levels in male rats. LSD, 0.20 mg/kg, also inhibits the increase in plasma PRL levels produced by chlorpromazine (CPZ), 5 mg/kg, and alpha-methyl-paratyrosine (AMPT), 50 mg/kg, both of which interfere with dopaminergic inhibition of PRL secretion. LSD was more potent than methysergide, a serotonin receptor blocker, in lowering plasma PRL levels and more potent than apomorphine, a known direct acting dopamine agonist, in blocking the increase in plasma PRL produced by quipazine, a 5-HT agonist. These results suggest LSD has potent dopamine agonist properties on the rat pituitary or hypothalamic dopamine receptors which directly or indirectly inhibit PRL secretion.

Animals↗
PubMed1960

Assay of lysergic acid diethylamide and its passage from blood into the perfused cerebral ventricles.

On the isolated rat uterus, lysergic acid diethylamide had an oxytocic action in a concentration of 2x10(-8); in smaller concentrations (10(-9) to 10(-10)), which had no stimulating effect of their own, it potentiated acetylcholine-induced contractions. This potentiating effect was made the basis for assaying minute amounts of lysergic acid diethylamide. The method was used to assay this substance in plasma of cats during its intravenous infusion at a rate of 10 mug./min./kg. During these infusions 0.4 to 2 ng./min. of lysergic acid diethylamide passed into the cerebral ventricles perfused with a salt solution of a composition resembling that of cerebrospinal fluid.

Acetylcholine↗
PubMed1974

Reversal learning enhanced by lysergic acid diethylamide (LSD): concomitant rise in brain 5-hydroxytryptamine levels.

1 Small doses of lysergic acid diethylamide (LSD) (12.5-50 mug/kg) consistently facilitated learning of a brightness discrimination reversal.2 2-Bromo-lysergic acid diethylamide (BOL-148), a structural analogue of LSD, with similar peripheral anti-5-hydroxytrypamine activity but no psychotomimetic properties, had no effect in this learning situation at a similar dose (25 mug/kg).3 LSD, but not BOL-148, caused a small but significant increase in brain 5-hydroxytryptamine levels, but had no effect on the levels of catecholamines in the brain at 25 mug/kg.

Animals↗
PubMed1999

Agonist-directed signaling of serotonin 5-HT2C receptors: differences between serotonin and lysergic acid diethylamide (LSD).

For more than 40 years the hallucinogen lysergic acid diethylamide (LSD) has been known to modify serotonin neurotransmission. With the advent of molecular and cellular techniques, we are beginning to understand the complexity of LSD's actions at the serotonin 5-HT2 family of receptors. Here, we discuss evidence that signaling of LSD at 5-HT2C receptors differs from the endogenous agonist serotonin. In addition, RNA editing of the 5-HT2C receptor dramatically alters the ability of LSD to stimulate phosphatidylinositol signaling. These findings provide a unique opportunity to understand the mechanism(s) of partial agonism.

3T3 Cells↗
PubMed1988

Antagonism of 5-hydroxytryptamine2 receptor-mediated phosphatidylinositol turnover by d-lysergic acid diethylamide.

The interactions of the indolealkylamine hallucinogen d-lysergic acid diethylamide (d-LSD) and two phenalkylamine hallucinogens, 2,5-dimethoxy-4-bromoamphetamine (DOB) and 2,5-dimethoxy-4-iodoamphetamine (DOI), with 5-hydroxytryptamine2 (5-HT2) receptors were analyzed in rat cortex using both radioligand binding techniques and biochemical measurements of phosphatidylinositol (PI) turnover. 5-HT2 binding sites were labeled by [3H]ketanserin. DOB and DOI displayed decreased affinity for 5-HT2 sites in the presence of 10(-4) M GTP, whereas the ability of d-LSD to compete for these sites was not affected by the presence of 10(-4) M GTP. Moreover, the Hill slope of the d-LSD competition curve was unity in both the absence and presence of 10(-4) M GTP. These findings suggest that d-LSD is an antagonist at 5-HT2 receptors. PI turnover studies in rat cortex showed that at 10(-5) M concentrations d-LSD, DOB and DOI display partial agonist activity in comparison to 10(-5) 5-HT. Stimulation of PI turnover by 5-HT, DOB and DOI was inhibited by the 5-HT2 antagonist ketanserin (10(-6) M). The d-LSD PI signal was not affected by the presence of ketanserin. In addition, nanomolar concentrations of d-LSD did not stimulate PI turnover in rat cortex. Moreover, nanomolar concentrations of d-LSD are able to significantly antagonize the stimulatory effect of 10(-5) M 5-HT on PI turnover. These data suggest that d-LSD acts as an antagonist at 5-HT2 receptors in rat cortex. At high concentrations (greater than 1 microM) d-LSD stimulates low-level PI turnover via a non-5-HT2 receptor-mediated mechanism.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗
PubMed1974

Mechanism of lysergic acid diethylamide interference with rabbit antibody biosynthesis.

Lymphoid cells from hyperimmune rabbits producing antibodies to a hapten, incubated in the presence of d-lysergic acid diethylamide, continued to synthesize protein at a normal rate. Isoelectric focusing analysis of the low-molecular-weight protein secreted by the cells incubated with lysergic acid diethylamide indicated two components, with pI's of 4.9 and 5.2. Immune cells not exposed to lysergic acid diethylamide secreted only 7S IgG molecules with an average pI of approximately 7.0.

Animals↗
PubMed1984

Ontogeny of the behavioral effects of lysergic acid diethylamide in cats.

The ontogeny of the behavioral effects of lysergic acid diethylamide (LSD) was examined in cats between the ages of 4 and 112 days postpartum. The kittens showed little LSD-induced behavioral change prior to 14 days of age. By the age of 21 days, however, the kittens exhibited many of the behavioral signs characteristic of LSD-induced behaviors in adult cats. These behaviors include limb-flicking, abortive grooming, head-shakes, grooming, and investigatory responses. In general, these behaviors began at a low frequency of occurrence, then increased rapidly with advancing age, reaching adult values by approximately 35-40 days of age, and remained relatively constant through 112 days postpartum. The time course for the behavioral effects following an acute injection of LSD showed the adult pattern, i.e., persisting for approximately 8 hr post-injection, from their earliest appearance during ontogeny. Young kittens (21-42 days of age) were resistant to the development of tolerance following repeated administration of the drug. LSD was capable of eliciting certain behaviors, such as head-shakes and grooming, well in advance of the age at which they normally appear spontaneously. This indicates that the neuronal and musculature substrata are developed for the performance of these behaviors long before the kitten naturally employs them.

Aging↗
PubMedDate not supplied

Optimization and immunological characterization of a photochemically coupled lysergic acid diethylamide (LSD) immunogen.

A photoreactive heterobifunctional linker was used to prepare an immunogen in which lysergic acid diethylamide was indirectly coupled to keyhole limpet hemocyanin at multiple sites on the drug. It was possible to attach approximately 35 drug molecules to each protein using approximately equal amounts of both species during the reaction. The presence of buffer components or water severely compromised reaction efficiency, as estimated from the molar substitution ratio. Factors such as excess linker, pH, irradiation of dry matrix in the absence of buffer, and the drug/protein ratio used during photolysis were shown to have pronounced effects on reaction efficiency. Structural insights regarding immunogen coupling were obtained by determining the specificities of antibodies which were raised against the immunogen. Cross-reactivity data indicated that haptenation of protein likely occurred at positions N1 and N6 of lysergic acid diethylamide, which is plausible given the electrophilicity of the photogenerated aryl nitrene.

Antibody Specificity↗
PubMed2000

Metabolism of lysergic acid diethylamide (LSD) to 2-oxo-3-hydroxy LSD (O-H-LSD) in human liver microsomes and cryopreserved human hepatocytes.

The metabolism of lysergic acid diethylamide (LSD) to 2-oxo-3-hydroxy lysergic acid diethylamide (O-H-LSD) was investigated in liver microsomes and cyropreserved hepatocytes from humans. Previous studies have demonstrated that O-H-LSD is present in human urine at concentrations 16-43 times greater than LSD, the parent compound. Additionally, these studies have determined that O-H-LSD is not generated during the specimen extraction and analytical processes or due to parent compound degradation in aqueous urine samples. However, these studies have not been conclusive in demonstrating that O-H-LSD is uniquely produced during in vivo metabolism. Phase I drug metabolism was investigated by incubating human liver microsomes and cryopreserved human hepatocytes with LSD. The reaction was quenched at various time points, and the aliquots were extracted using liquid partitioning and analyzed by liquid chromatography-mass spectrometry. O-H-LSD was positively identified in all human liver microsomal and human hepatocyte fractions incubated with LSD. In addition, O-H-LSD was not detected in any microsomal or hepatocyte fraction not treated with LSD nor in LSD specimens devoid of microsomes or hepatocytes. This study provides definitive evidence that O-H-LSD is produced as a metabolic product following incubation of human liver microsomes and hepatocytes with LSD.

Chromatography, Liquid↗
PubMed1958

The effect of (+)-lysergic acid diethylamide and other drugs on the carotid sinus reflex.

In cats, lysergic acid diethylamide (LSD) selectively blocked the reflex blood pressure rise following carotid chemoreceptor stimulation. It also reduced or abolished the chemoreceptor component of the pressor response to occlusion of the common carotid arteries. It did not inhibit the respiratory reflexes arising from the carotid chemoreceptors, unless spontaneous respiration was interfered with as a whole. The site of action was central, probably below the intercollicular level, regardless of whether the drug was administered by the intravenous route or into the lateral ventricle of the brain.LSD did not block the baroreceptor depressor reflex elicited by stimulation of one carotid sinus nerve. LSD frequently caused the systemic pressure to fall, even after vagotomy and atropine, and this effect might account for the occasional reduction of the baroreceptor component of the carotid occlusion response. On the other hand, no relationship was found between the action of LSD on vasomotor tone and its blocking effect on the chemoreceptor pressor reflex.Some derivatives of LSD produced effects similar to those described for LSD, whether or not they possessed a psychotropic action in man, and independently of their efficiency as antagonists to 5-hydroxytryptamine. Of a series of compounds chemically unrelated to LSD, chlorpromazine was found to block the chemoreceptor pressor rise after intracerebroventricular injection.

Animals↗
PubMed1975

Interactions between lysergic acid diethylamide and dopamine-sensitive adenylate cyclase systems in rat brain.

Investigations were carried out on the interactions of the hallucinogenic drug, D-lysergic acid diethylamide (D-LSD), and other serotonin antagonists with catecholamine-sensitive adenylate cyclase systems in cell-free preparations from different regions of rat brain. In equimolar concentration, D-LSD, 2-brono-D-lysergic acid diethylamide (BOL), or methysergide (UML) strongly blocked maximal stimulation of adenylate cyclase activity by either norepinephrine or dopamine in particulate preparations from cerebral cortices of young adult rats. D-LSD also eliminated the stimulation of adenylate cyclase activity of equimolar concentrations of norepinephrine or dopamine in particulate preparations from rat hippocampus. The effects of this hallucinogenic agent on adenylate cyclase activity were most striking in particulate preparations from corpus striatum. Thus, in 10 muM concentration, D-LSD not only completely eradicated the response to 10 muM dopamine in these preparations but also consistently stimulated adenylate cyclase activity. L-LSD (80 muM) was without effect. Significant activation of striatal adenylate cyclase was produced by 0.1 muM D-LSD. Activation of striatal adenylate cyclase of either D-LSD or dopamine was strongly blocked by the dopamine-blocking agents trifluoperazine, thioridazine, chlorpromazine, and haloperidol. The stimulatory effects of D-LSD and dopamine were also inhibited by the serotonin-blocking agents, BOL, 1-methyl-D-lysergic acid diethylamide (MLD), and cyproheptadine, but not by the beta-adrenergic-blocking agent, propranolol. However, these serotonin antagonists by themselves were incapable of stimulating adenylate cyclase activity in the striatal preparations. Several other hallucinogens, which were structurally related to serotonin, were also inactive in this regard, e.g., mescaline, N,N-dimethyltryptamine, psilocin and bufotenine. Serotonin itself produced a small stimulation of adenylate cyclase activity in striatal preparations and, in relatively high concentration (100 muM), partially blocked the activation by 10 muM dopamine, but was without effect on the stimulation by 10 muM D-LSD. The present results indicate that serotonin antagonists, in general, are potent inhibitors of catecholamine-induced stimulation of adenylate cyclase systems in brain cell-free preparations. In addition, these results, coupled with earlier findings on the capacity of D-LSD to interact with serotonin-sensitive adenylate cyclase systems from rat brain23,24 and other neural systems16, strongly suggest that this hallucinogenic agent is capable of acting as an agonist at central dopamine and serotonin receptors, as well as functioning as an antagonist at dopamine, norepinephrine, and serotonin receptors in the brain.

Adenylyl Cyclases↗