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Results for “LYSERGIC ACID DIETHYLAMIDE”

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PubMed1980

d-[3H]Lysergic acid diethylamide binding to serotonin receptors in the molluscan nervous system.

d-[3H]Lysergic acid diethylamide (LSD) bound to both dopamine- and serotonin (5HT)-sensitive sites in a particulate fraction derived from the central nervous system of the snail Helix pomatia. Conditions were found which enabled the two sites to be studied independently. [3H]LSD appeared to have a slightly higher affinity for dopamine-sensitive binding (Kd = 0.5 nM) than for 5HT-sensitive binding (Kd = 1.2 nM). A pharmacological analysis of the binding indicated that while dopamine- and 5HT-related agonists clearly discriminated between the two sites, putative antagonists showed little specificity for dopamine- or 5HT-sensitive binding. The pharmacology of 5HR-sensitive [3H]LSD binding was studied in relation to a 5HT-sensitive adenylate cyclase present in a particulate fraction derived from the same tissue. There was a very good correlation between the abilities of a range of agents to act as agonists or antagonists in the 5HT-sensitive adenylate cyclase assay and their abilities to displace 5HT-sensitive [3H]LSD binding (r = 0.94; p less than 0.001). In particular, d-LSD and a number of neurologic drugs were inhibitory in both assays in a stereoselective manner. These data suggest that in molluscan tissues, 5HT-sensitive [3H]LSD binding is related to the 5HT receptor which is coupled to adenylate cyclase.

Adenylyl Cyclases↗
PubMed1976

Tolerance and limited cross-tolerance to the effects of N, N-dimethyltryptamine (DMT) and lysergic acid diethylamide-25 (LSD) on food-rewarded bar pressing in the rat.

Lysergic acid diethylamide=25 (LSD) and N,N-dimethyltryptamine (DMT) abolish food-rewarded, fixed-ratio bar pressing by rats in a dose-related fashion. Adult male Holtzman rats trained to press a bar (respond) for milk reward on a 4-response fixed-ratio schedule were given i.p. injections of 3.2 or 10 mg/kg of DMT every 2 hours for 21 days. Every 24 hours the animals were placed in operant chambers for 30 minutes before a scheduled injection and were left in the chambers for 30 to 80 minutes after. During the first week of chronic treatment, daily bar pressing worsened progressively until the 6th day of the series, at which time rats in the 10 mg/kg group did not bar press at all. As the chronic injections continued, rates of bar pressing gradually increased until responding was not disrupted at all by an injection of DMT. Rats in the 3.2 mg/kg group showed cross-tolerance to an injection of LSD (0.1 mg/kg). Another group of rats was made partially tolerant to the disruptive effects of LSD (0.1 mg/kg i.p.) on bar pressing with a series of injections given once per day for 21 days and then three times per day for the next 4 days. Cross tolerance was not demonstrated to a challenge injection of 10 mg/kg of DMT. The LSD injections were continued for another 3 to 5 days until the animals were completely tolerant to the LSD. They then displayed cross-tolerance to 3.2 mg/kg of DMT.

Animals↗
PubMed1977

Lysergic acid diethylamide. Photoelectron ionization potentials as indices of behavioral activity.

The photoelectron spectrum of lysergic acid diethylamide (LSD) reveals five ionization potentials (IP's) between 7.25 and 9.75 eV arising from the aromatic (pi) portion of the molecule and IP's of 8.4 eV arising from the tertiary amine and 8.5-9.0 and 9.1 eV arising from the amide group. Comparisons of the IP's of LSD, and of phenethylamines and tryptamines reported by us elsewhere, with activities of these compounds in rat and human behavioral tests show that increasing activity is paralleled by decreasing IP.

Animals↗
PubMed1957

The effect of lysergic acid diethylamide, 5-hydroxytryptamine, and related compounds on the liver fluke, Fasciola hepatica.

The rhythmical activity of the liver fluke, Fasciola hepatica, was stimulated by 5-hydroxytryptamine and by lysergic acid diethylamide at very low concentrations. The effect was peripheral and was not mediated through the central ganglion. Other amines also stimulated rhythmical activity, the most potent being the indolamines.Bromolysergic acid diethylamide, and other analogues such as yohimbine, harmine, and dopamine depressed rhythmical movement and antagonized the stimulant action of 5-hydroxytryptamine and lysergic acid diethylamide. Evidence which suggests the presence of tryptamine receptors in the trematode is discussed.

Animals↗
PubMed1983

Photoreactivity of lysergic acid diethylamide and its possible utility as a photoaffinity labeling reagent.

Aqueous solutions of lysergic acid diethylamide (LSD) are extremely sensitive to light in the near-ultraviolet region of the spectrum. This rather efficient photoreaction yields a variety of products which have very low affinity for LSD-binding sites on plasma membranes from Fasciola hepatica. Since this photoreaction may be elicited by normal white fluorescent lighting in the laboratory, it represents a potential source of error in determining the binding affinity of LSD. Utilizing this photoreactivity advantageously, [3H]LSD was used to photolabel membrane proteins. Covalent binding of [3H]LSD was shown to be a function of the duration of illumination and was inhibited by 5-hydroxytryptamine and nonradioactive LSD. Sodium dodecylsulfate (SDS) polyacrylamide gel electrophoresis of [3H]LSD labeled membranes from F. hepatica showed two proteins which were selectively labeled by the photoreactive [3H]LSD. This method of direct photolabeling with non-derivatized [3H]LSD may allow identification of LSD-binding proteins in a variety of systems.

Affinity Labels↗
PubMed1989

Increased serotonin2 (5-HT2) receptor binding as measured by 3H-lysergic acid diethylamide (3H-LSD) in the blood platelets of depressed patients.

3H-Lysergic acid diethylamide (3H-LSD) binding, a putative measure of 5-HT2 receptor binding, was studied in the blood platelets of 29 depressed patients and 24 normal controls. The Bmax (maximum number of 3H-LSD binding sites) in the blood platelets of depressed patients was significantly greater than that of normal volunteers. This increase in Bmax was due to an increase in female depressed patients only. Bmax was significantly lower in female compared to male normal controls but there was no difference between male and female depressed patients. There was also no difference in Kd (an inverse measure of affinity of 3H-LSD binding to its sites) between normal controls and depressed patients. The correlations between Bmax of 3H-LSD binding and the Bmax of the 3H-imipramine binding site or the Vmax of 5-HT uptake sites were not significant. The role of serotonergic processes in the psychobiology of depression is discussed.

Adult↗
PubMed2002

A single dose of lysergic acid diethylamide influences gene expression patterns within the mammalian brain.

Hallucinogenic drugs such as lysergic acid diethylamide (LSD) have profound effects on humans including hallucinations and detachment from reality. These remarkable behavioral effects have many similarities to the debilitating symptoms of neuropsychiatric disorders such as schizophrenia. The effects of hallucinogens are thought to be mediated by serotonin receptor activation; however, how these drugs elicit the unusual behavioral effects remains largely a mystery, despite much research. We have undertaken the first comprehensive analysis of gene expression influenced by acute LSD administration in the mammalian brain. These studies represent a novel approach to elucidate the mechanism of action of this class of drugs. We have identified a number of genes that are predicted to be involved in the processes of synaptic plasticity, glutamatergic signaling and cytoskeletal architecture. Understanding these molecular events will lead to new insights into the etiology of disorders whose behavioral symptoms resemble the temporary effects of hallucinogenic drugs, and also may ultimately result in new therapies.

Animals↗
PubMedDate not supplied

Genetic toxicology of lysergic acid diethylamide (LSD-25).

The acute and the chronic psychotomimetic potentials of the hallucinogen lysergic acid diethylamide (LSD-25) have been recognized for almost 40 years. That additional types of the biological effects should have come under scrutiny was directly attributable to widespread use and abuse of this drug on a world-wide basis. Although "genetic toxicology" encompasses a broad spectrum of disciplines, including many areas of highly specialized research, perhaps the most germane, and those on which this review has concentrated, are Clastogenicity, Mutagenicity, Teratogenicity and Oncogenicity. Based on our current understanding and interpretation of the available data, the genetic toxicology of LSD provides an excellent example of Newton's "third law of motion", e.g., to every force there is an equal and opposite reaction force. From the published material it is impossible to draw clear cut conclusions regarding any of the above "problem areas" in spite of the considerable scientific effort invested. Most of the in vitro studies performed on the clastogenicity of LSD indicate either suppression of mitosis or enhanced chromosome damage. However, extrapolation of such results to the in vivo situation is very difficult. With regard to in vivo human use of the drug, no concensus is attainable as to chromosome breakage and the inconsistencies within and between studies remain inexplicable. However, several of the "controlled" investigations assessing the in vivo effect of chemically pure LSD suggest a transient increase in lymphocyte chromosome breakage. On the other hand, the results of cytogenetic studies on experimental animals are contradictory. Although human studies are nonexistent, in those experimental organisms tested, using accepted techniques, LSD proved to be, at best, a weak mutagen, if mutagenic at all. Teratogenicity studies in animals are confusing due to the multitude of organisms and plethora of discriminant parameters studied. However, with regard to man there has been ample opportunity and one can conclude that LSD is not teratogenic. As to the drug's oncogenic potential, the 3 reported cases of leukemia in LSD users are most likely the result of coincidence.

Animals↗
PubMed1968

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.

Animals↗
PubMed1997

Gas chromatographic/mass spectrometric determination of lysergic acid diethylamide (LSD) in serum samples.

A sensitive method for the detection and quantification of lysergic acid diethylamide (LSD) in serum samples is described. After liquid-liquid extraction the trimethylsilyl derivative of LSD is detected by gas chromatography-mass spectrometry. Experiments with spiked samples resulted in a recovery of 76%, the coefficient of variation was 9.3%. Excellent linearity was obtained over the range 0.1-10 ng ml-1. Additionally experiments demonstrating the light sensitivity of LSD are presented together with casuistics.

Adolescent↗