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PubMed1961

10-Methoxyharmalan, a potent serotonin antagonist which affects conditioned behavior.

10-Methoxyharmalan, an alkaloid obtained by the cyclodehydration of melatonin, itself a derivative of serotonin, is a more potent serotonin antagonist than harmaline and is only slightly less active than lysergic acid diethylamide. It has a similar, yet slightly greater, effect on behavior as that of harmaline and is the most potent serotonin derivative, so far tested, that affects the avoidance-escape behavioral reflex

Lysergic Acid Diethylamide↗
PubMed1957

The antagonism of the vascular effects of 5-hydroxytryptamine by BOL 148 and sodium salicylate in the human subject.

2-Bromo-(+)-lysergic acid diethylamide (BOL 148) is a specific antagonist of the constrictor response of the forearm and hand blood vessels to intra-arterial infusions of 5-hydroxytryptamine. This has been shown to be a direct action in the tissue concerned, since the antagonism was as effective when the drug was given by local arterial injection as when given intravenously. Sodium salicylate is also a specific antagonist of 5-hydroxytryptamine, but its action is indirect, occurring only when the general serum level was raised above 10 or 20 mg.%; local limb concentrations of 30 to 40 mg.% had no antagonistic effect. The mechanism of the antagonistic effect of salicylate is not known. It is not related to the associated hyperventilation but is possibly due to the secondary release of, or synergism with, some other substance, probably a hormone.

Blood Vessels↗
PubMed1969

On the conformations of hallucinogenic molecules and their correlation.

There are only a few possible conformations of D-lysergic acid diethylamide and hallucinogenic derivatives of tryptamine and phenylethylamine. Of these possible conformations there is a high structural correlation among the probable conformations of active hallucinogenic molecules and between these conformations and the known conformations of several central nervous system transmitter molecules.

Chemistry, Pharmaceutical↗
PubMed1961

Multiple toe-pinch method for testing analgesic drugs.

In guinea-pigs and rats, an immediate squeak was one of the most consistent and readily observed responses to application of a light artery clip to the base of a toe. Morphine and related drugs suppressed this response. Squeak-responses from each toe of an experimental animal formed the basis of a technique for measuring activity of analgesic drugs. A statistical method was developed to analyse the correlated quantal observations obtained. It provided an estimate of the increase of information from several toes compared with one. Testing all toes of each animal yielded a substantial increase of information, because the correlation between responses of different toes was low. Among drugs having an analgesic action in man, 1-(beta-diethyl-aminoethyl)-2-(p-ethoxybenzyl)-5-nitrobenzimidazole, methadone, morphine, pethidine and codeine (in descending order of potency) were active in this test in guinea-pigs. Acetylsalicylic acid, amidopyrine, amphetamine, chlorpromazine, 4-hydroxyisophthalic acid, lysergic acid diethylamide, mephenesin, nalorphine, pentetrazole, phenobarbitone, phencyclidine, phenytoin, salicylamide, strychnine and troxidone showed little or no activity. The time-courses of active drugs were estimated, and morphine had the longest action.

Aminopyrine↗
PubMed1972

Molecular structure of LSD.

The molecular configuration of lysergic acid diethylamide (LSD) in crystals of the iodobenzoate has been determined by using x-ray diffraction techniques. The configuration shows strain and steric hindrance and the conformation is fixed. Some of the implications of this for the hallucinogenic activity of LSD are discussed.

Lysergic Acid Diethylamide↗
PubMed1992

Serotonergic aspects of the response of human platelets to immune-adjuvant muramyl dipeptide.

The human platelet serotonergic responses of aggregation and uptake were shown to be modulated by muramyl peptides. Muramyl dipeptide inhibited serotonin uptake in a temperature dependent and stereospecific manner. It also blocked the binding to platelets of [3H]imipramine, a well-known inhibitor of serotonin uptake. Muramyl dipeptide decreased serotonin2 (5-HT2) mediated platelet aggregation, and blocked the binding of a 5-HT2-specific ligand: lysergic acid diethylamide. Since muramyl peptides are released upon degradation of bacteria, the findings offer a possible mechanism for neuro-immune modulation by emphasizing the interaction between 5-HT (a neurotransmitter) and muramyl peptides (immuno-adjuvants).

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1957

Two kinds of tryptamine receptor.

There are two kinds of tryptamine receptor in the guinea-pig ileum, namely the M receptors which can be blocked with morphine and the D receptors which can be blocked with dibenzyline. Atropine, an atropine-like drug, cocaine, and methadone inhibit effects due to the M receptors, even after dibenzyline, but have no additional effect after morphine. Lysergic acid diethylamide, dihydroergotamine and 5-benzyloxygramine inhibit effects due to the D receptors, even after morphine, but have no additional effect after dibenzyline. The M receptors are probably in the nervous tissue and the D receptors are probably in the muscles.

Alkaloids↗
PubMed1979

An improved method for detecting drug effects in the open field.

A double test cross-over design was applied to the testing of rats in the open field. When used to examine the effects of atropine, chlorpromazine and lysergic acid diethylamide (LSD) on open field behaviour, this design proved 4--40 times more sensitive than the previously popular single test design. In no case was the double test design less sensitive. Results are discussed in relation to screening of medically useful compounds.

Animals↗
PubMed1981

Modification of apomorphine hypothermia by drugs affecting brain 5-hydroxytryptamine function.

Intraperitoneal administration of apomorphine caused hypothermia in mice. Pretreatment with the serotonin (5-HT) receptor antagonists methysergide (3 mg/kg), cinanserin (10 mg/kg) or brom-LSD (3 mg/kg) potentiated this response of apomorphine. Brain 5-HT depletion by p-chlorophenylalanine caused similar modification. On the contrary, the 5-HT receptor agonists quipazine (3 mg/kg) and MK-212 (3 mg/kg), significantly blocked apomorphine hypothermia. It was concluded that 5-HT modulates the dopamine (DA)-mediated body temperature changes and that drug-induced alterations in the brain 5-HT function modify apomorphine-induced hypothermia in a predictable manner. One mg/kg dose of lysergic acid diethylamide (LSD) blocked apomorphine hypothermia. The apomorphine-blocking effect of both quipazine and LSD developed tolerance. Moreover, LSD showed cross tolerance with quipazine. It was concluded that the hypothermia-blocking property of LSD resides on its ability to activate the hypothalamic 5-HT receptors.

Animals↗
PubMed1987

Enhancement of recurrent inhibition of the spinal monosynaptic reflex by preceding stimulation of the medullary raphé in rats.

Recurrent inhibition of the spinal monosynaptic reflex (MSR) elicited by conditioning stimulation of the ventral root in anesthetized rats was weaker than both the recurrent inhibition of the disynaptic reflex and the inhibition of the MSR elicited by conditioning stimulation of the adjacent dorsal root. Among these 3 inhibitions, the recurrent inhibition of the MSR was enhanced to a markedly greater extent by a preceding stimulation of the medullary raphé nucleus than were the other inhibitions. The magnitude of the enhancement of the recurrent inhibition of MSR also was much greater when the medullary stimulation was delivered 20 ms prior to the ventral root activation, as compared with a 30-ms interval. Recurrent inhibition of the MSR was enhanced by intravenous injection of lysergic acid diethylamide (LSD); however, the enhanced effect on recurrent inhibition elicited by stimulation of the raphé nucleus was not attenuated by the drug. These results suggest that there is a non-serotonergic, descending pathway which is capable of modulating motor output solely by means of recurrent inhibition of the MSR.

Animals↗
PubMed2006

Ergot and its alkaloids.

This manuscript reviews the history and pharmacognosy of ergot, and describes the isolation/preparation, chemistry, pharmacodynamics, and pharmacotherapeutics of the major ergot alkaloids and their derivatives. A brief discussion of the hallucinogenic properties of lysergic acid diethylamide is also featured. An abbreviated form of the material found in this paper is presented in a 4-hour didactic format to third-professional year PharmD students as part of their study of vascular migraine headaches, Parkinson's disease, and naturally occurring hallucinogens/hallucinogen derivatives in the modular course offering Neurology/Psychiatry.

Animals↗
PubMed1968

LSD in mice: abnormalities in meiotic chromosomes.

Meiotic chromosomes of six mice injected with high doses of lysergic acid diethylamide (LSD-25) and of six controls were studied. Several breaks, gaps, and unidentifiable fragments were found in the treated but, with a few exceptions, not in the control animals. Secondary constrictions were more numerous in the treated than in the untreated mice. Possible consequences are discussed.

Animals↗
PubMed2000

Prior experience of morphine application alters the c-fos response to MDMA ('ecstasy') and cocaine in the rat striatum.

Repeated morphine application usually leads to the development of tolerance but under certain circumstances sensitization may arise simultaneously. This phenomenon becomes obvious in behavioral tests as increasing locomotor activity and increasing drug self-administration during a course of chronic morphine application. It was suggested recently that sensitization could contribute to addiction. The molecular mechanisms of sensitization may include the long lasting increase in neuronal responsiveness to morphine which was observed in defined brain areas after repeated morphine injections. In this work, we studied whether morphine-sensitized Wistar rats also display an enhanced neuronal activity in response to other drugs of abuse (so called co-sensitization). The substances to be tested were injected as single doses 4 weeks after completion of a 10-day morphine pretreatment. MDMA (3, 4-methylenedioxymethamphetamine, 6 mg/kg) as a single test dose yielded a c-fos response in a wide range of brain areas. In the caudate putamen, the expression pattern of c-fos was clearly altered if the rats had received repeated morphine application previously. In this case, the MDMA-induced c-fos expression was markedly confined to the centromedial, mesolimbic aspect of the striatum whereas it had a diffuse appearance in rats not exposed to the opiate earlier. Cocaine application (50 mg/kg) elicited an intense c-fos expression in the medial striatum if the animals were morphine-pretreated; it was virtually absent in drug-naive rats after the same cocaine dose. Ten mg/kg cocaine had a similar but weaker effect. No difference in the c-fos expression pattern between morphine and saline pretreated animals was observed in the case of a THC (Delta(9)-tetrahydrocannabinol, 25 mg/kg) or an LSD (lysergic acid diethylamide, 1 mg/kg) test application. These findings imply that morphine sensitizes the brain towards other addicting drugs. In consequence, morphine sensitization obviously does not solely reflect alterations in mu-opioid receptor signaling. Rather, it seems to reflect further rearrangements within the mesolimbic system.

Animals↗
PubMed1985

5-Hydroxytryptamine mediates inhibitory postsynaptic potentials in rat dorsal raphe neurons.

In rat dorsal raphe neurons, focal electrical stimulation elicited a slow inhibitory postsynaptic potential (IPSP) associated with increased membrane conductance. On the basis of data in the literature this IPSP is presumably caused by a recurrent inhibitory circuit. 5-Hydroxytryptamine (5-HT) application caused a hyperpolarization of the cell membrane, also associated with increased membrane conductance. Both responses could be abolished by lysergic acid diethylamide or methysergide, and enhanced by imipramine. The reversal potentials for the responses were at the same level of - 95 mV which suggests an increase in membrane potassium conductance as the mechanism of both responses. These data suggest that 5-HT may be the mediator of the IPSP evoked by focal stimulation.

Animals↗
PubMed2002

Identification of a dopamine receptor from Caenorhabditis elegans.

The neurotransmitter dopamine regulates locomotion and egg laying in the nematode Caenorhabditis elegans. We have cloned a cDNA encoding the C. elegans G protein-coupled receptor (CeDOP1). The deduced amino acid sequence of the cloned cDNA shows high sequence similarities with D1-like dopamine receptors from other species. Three splice variants that differ in the length of the predicted third intracellular loop and C-terminal tail were identified. COS-7 cells transiently transfected with CeDOP1 showed high affinity binding to [(125)I]iodo-lysergic acid diethylamide (K(D)=3.43 +/- 0.83 nM). Dopamine showed the highest affinity (K(i)=0.186 microM) for this receptor among several vertebrate and invertebrate amine neurotransmitters tested, suggesting that the natural ligand for this receptor is dopamine.

Animals↗
PubMed1961

Antagonism of apomorphine-induced pecking in pigeons.

Central nervous system stimulants, tranquillizers and other central nervous system depressants, antiemetics, antihistamine drugs and autonomic blocking agents were examined for their ability to prevent the pecking response in pigeons induced by apomorphine (250 mug/kg intramuscularly). Reduction in the proportion of positive responses or significant increase in the latent period of pecking were taken as the criterion of effectiveness. Protection was afforded by caffeine, lysergic acid diethylamide, morphine, rauwolscine, triflupromazine and yohimbine. In addition, a significant increase in latent period was produced by artane, pentobarbitone, benactyzine, 2-bromolysergic acid diethylamide, cyclizine, diphenhydramine, ergotoxine, hyoscine, promethazine, 5-(2-chloroethyl)-4-methylthiazole and trimethobenzamide. Most of these drugs influenced the pecking and emetic responses to apomorphine in an identical manner. It is possible that identical receptors may be concerned with apomorphine pecking (in pigeons) and emesis (in other species).

Animals↗
PubMed1987

Distribution of neurotransmitter binding sites in the cat median eminence.

Receptor autoradiography was used to determine the distribution of binding sites for monoaminergic and cholinergic neurotransmitters in the cat median eminence. Results showed that binding sites were differentially distributed in that [3H]-p-aminoclonidine (an alpha-2-adrenergic ligand) and [3H]pyrilamine (an H1-histaminergic ligand) binding were concentrated in the medial region of the external layer of the median eminence while [3H]lysergic acid diethylamide (a serotonergic ligand) and [3H] quinuclidinyl benzilate (a muscarinic cholinergic ligand) binding were concentrated within the lateral region of the external layer. These patterns are coincident with the differential distribution of hypophysiotropic hormones in the median eminence, suggesting that monoamines and acetylcholine may regulate the release of these hormones at the level of the median eminence.

Animals↗