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PubMed1976

Comparison of the action of lysergic acid diethylamide and apomorphine on the copulatory response in the female rat.

The effects of lysergic acid diethylamide (LSD) and apomorphine were compared using female copulatory behavior (lordosis response), in ovariectomized estrogen + progesterone-treated rats. Both serotonin and dopamine are implicated in the inhibition of this behavior. Each compound inhibited lordosis behavior dose dependently and with a similar time-course. Pimozide (0.1; 0.5 mg/kg) blocked the apomorphine (0.2 mg/kg)-induced decrease of lordosis response, while only a certain abbreviation of the LSD (0.10 mg/kg) inhibition was achieved by pimozide (0.5 mg/kg). Chlorpromazine (0.5 mg/kg) in a dose without effects on lordosis of its own had an action similar to pimozide on the LSD effect. It is concluded that the predominant action of LSD on the female copulatory response is not mediated by increased dopamine receptor activity but that the LSD effect might be modulated by decreased dopaminergic activity.

Animals↗
PubMed1990

Lysergic acid diethylamide (LSD) administration selectively downregulates serotonin2 receptors in rat brain.

A dosage regimen of lysergic acid diethylamide (LSD) that reliably produces behavioral tolerance in rats was evaluated for effects on neurotransmitter receptor binding in rat brain using a variety of radioligands selective for amine receptor subtypes. Daily administration of LSD [130 micrograms/kg (0.27 mumol/kg) intraperitoneally (IP)] for 5 days produced a decrease in serotonin2 (5-hydroxytryptamine2, 5-HT2) binding in cortex (measured 24 hours after the last drug administration) but did not affect binding to other receptor systems (5-HT1A, 5-HT1B, beta-adrenergic, alpha 1- or alpha 2-adrenergic, D2-dopaminergic) or to a recognition site for 5-HT uptake. The decrease was evident within 3 days of LSD administration but was not demonstrable after the first LSD dose. Following 5 days of LSD administration the decrease was still present 48 hours, but not 96 hours, after the last administration. The indole hallucinogen psilocybin [1.0 mg/kg (3.5 mumol/kg) for 8 days] also produced a significant decrease in 5HT2 binding, but neither the nonhallucinogenic analog bromo-LSD [1.3 mg/kg (2.4 mumol/kg) for 5 days] nor mescaline [10 mg/kg (40.3 mumol/kg) for 5 or 10 days] affected 5-HT2 binding. These observations suggest that LSD and other indole hallucinogens may act as 5-HT2 agonists at postsynaptic 5-HT2 receptors. Decreased 5-HT2 binding strikingly parallels the development and loss of behavioral tolerance seen with repeated LSD administration, but the decreased binding per se cannot explain the gamut of behavioral tolerance and cross-tolerance phenomena among the indole and phenylethylamine hallucinogens.

Animals↗
PubMed1970

Iontophoretic release of acetylcholine, noradrenaline, 5-hydroxytryptamine and D-lysergic acid diethylamide from micropipettes.

1. The in vitro iontophoretic release of tritium-labelled acetylcholine and 5-hydroxytryptamine from large and small micropipettes and noradrenaline and D-lysergic acid diethylamide from small micropipettes was determined by liquid scintillation counting.2. The release was directly proportional to the electrical charge passed in the range normally used in the iontophoretic study of these compounds. The transport numbers obtained for the large micropipettes were approximately double those with the small micropipettes. A very low transport number was found for D-lysergic acid diethylamide.3. The spontaneous leakage was small and did not vary appreciably with time.4. The iontophoretic release of acetylcholine in vitro agreed with the in vitro measurements.5. The brain-stem tissue concentration of D-lysergic acid diethylamide after intravenous injection into intact and decerebrate cats was determined.

Acetylcholine↗
PubMed1992

Chromatographic and mass spectrometric methods for determination of lysergic acid diethylamide (LSD) and metabolites in body fluids.

Continued illicit use of the potent psychedelic drug lysergic acid diethylamide (LSD) has stimulated efforts to develop effective analytical methods for detection of the drug and its metabolites in body fluids from suspected LSD users. Recently reported methods based on gas and liquid chromatography, combined with single- and multiple-stage mass spectral analysis, now permit accurate detection and quantitation of LSD at sub-nanogram/milliliter concentrations.

Body Fluids↗
PubMed1980

Behavioral thermoregulation in rats during hyperthermia induced by lysergic acid diethylamide.

In free moving rats trained to press a bar to escape from radiant heat, lysergic acid diethylamide (LSD, 8-16 micrograms) produced a significant and dose-dependent increase of the bar-pressing rate when injected intraperitoneally. During the increase in the bar-pressing rate, the rectal temperature showed an increase and both the tail-skin and the ambient temperature selected decreased concomitantly. The results indicate that LSD-induced hyperthermia is not due to an upward setting of the thermostat but mediated through the action of LSD on the effector pathways in the rats.

Animals↗
PubMed1986

Effects of repeated administration of the monoamine oxidase inhibitor phenelzine on the discriminability of d-lysergic acid diethylamide (LSD) and 1-(m-trifluoromethylphenyl) piperazine (TFMPP).

Rats trained to discriminate d-lysergic acid diethylamide (LSD; 0.08 mg/kg) or 1-(m-trifluoromethylphenyl) piperazine (TFMPP; 0.8 mg/kg) were treated with the monoamine oxidase inhibitor (MAOI) phenelzine (10 mg/kg/day) for 7 days. After a 24 h "washout" period, they were challenged with the training drug (and dose) or saline, during extinction test sessions. Following 0.08 mg/kg LSD, LSD-trained rats responded primarily on the saline lever (29% drug-appropriate responding) while, after TFMPP (0.8 mg/kg), TFMPP-trained animals responded on the drug lever (75% drug-appropriate responding). These preliminary data suggest that, if serotonin receptors are involved in the behavioral effects of TFMPP, these receptors differ from those involved in the effects of LSD.

Animals↗
PubMed1985

125I-lysergic acid diethylamide binds to a novel serotonergic site on rat choroid plexus epithelial cells.

125I-Lysergic acid diethylamide (125I-LSD) binds with high affinity to serotonergic sites on rat choroid plexus. These sites were localized to choroid plexus epithelial cells by use of a novel high resolution stripping film technique for light microscopic autoradiography. In membrane preparations from rat choroid plexus, the serotonergic site density was 3100 fmol/mg of protein, which is 10-fold higher than the density of any other serotonergic site in brain homogenates. The choroid plexus site exhibits a novel pharmacology that does not match the properties of 5-hydroxytryptamine-1a (5-HT1a), 5-HT1b, or 5-HT2 serotonergic sites. 125I-LSD binding to the choroid plexus site is potently inhibited by mianserin, serotonin, and (+)-LSD. Other serotonergic, dopaminergic, and adrenergic agonists and antagonists exhibit moderate to weak affinities for this site. The rat choroid plexus 125I-LSD binding site appears to represent a new type of serotonergic site which is located on non-neuronal cells in this tissue.

Animals↗
PubMed1984

Characterisation of [3H]lysergic acid diethylamide binding to a 5-hydroxytryptamine receptor on human platelet membranes.

Specific binding of [3H]lysergic acid diethylamide (LSD) to human platelet membranes, as defined by 300 nM spiperone, was saturable over the concentration range of 0.25-2.5 nM [3H]LSD. At 0.5 nM [3H]LSD the half-time for association at 37 degrees C was 56 min, half-time for dissociation was 173 min, and the kinetically derived affinity was 0.24 nM. In 19 control subjects equilibrium binding studies gave an affinity of 0.53 +/- 0.02 nM (mean +/- S.E.M.) and capacity of 57.1 +/- 5.6 fmol/mg protein (mean +/- S.E.M.). The inhibition profile was consistent with that of a 5-hydroxytryptamine (5-HT) receptor. There was a significant correlation between the inhibition of [3H]LSD binding and the inhibition of 5-HT-induced shape change, but not inhibition of active platelet uptake of 5-HT. There was also a significant correlation between the inhibition of [3H]LSD binding to human platelet membranes and human frontal cortex. Platelet [3H]LSD binding may therefore be a useful model for study of peripheral and central 5-HT receptors in man.

Binding Sites↗
PubMed1985

Discriminative stimulus properties of lysergic acid diethylamide in the monkey.

Four monkeys (Cercopithecus aethiops) were trained to discriminate 0.06 mg/kg of lysergic acid diethylamide (LSD) from saline in a two-key task in which correct responding was reinforced with food under a fixed ratio 32 schedule. The ED50 of LSD was 0.011 mg/kg. The nonhallucinogenic ergot, lisuride, and the hallucinogen, 5-methoxy-N,N-dimethyltryptamine, substituted completely for LSD (ED50 values were 0.0098 and 0.45 mg/kg, respectively). Mescaline (1-40 mg/kg), d-amphetamine (0.1-0.625 mg/kg) and apomorphine (0.1-0.5 mg/kg) did not substitute for LSD. In antagonism testing with ketanserin (1-10 mg/kg) or pirenperone (0.025 and 0.05 mg/kg), only the highest dose of pirenperone attenuated the LSD stimulus effect (to 55%). A 0.1-mg/kg dose of pirenperone produced nonresponding in three of four animals. The LSD cue was unaffected by clozapine (1 and 2 mg/kg), haloperidol (0.1 mg/kg) and pizotifen (0.6-1.8 mg/kg). The fact that lisuride does not readily cause hallucinations in humans, but yet substituted for LSD in primates, indicates that the LSD cue may not reflect the hallucinogenic properties of LSD. It is suggested that the LSD stimulus effect may depend on receptors (e.g., serotonergic) that, at the moment, are only poorly characterized.

Animals↗
PubMed1983

Differential effects of lysergic acid diethylamide, methysergide, and cyproheptadine on modality-specific and nonspecific sensory evoked potentials.

The effects of lysergic acid diethylamide (LSD), methysergide, and cyproheptadine on activity in classical primary pathways of the visual and somatosensory systems were compared with their effects on activity in sensory convergent (association) regions in alpha-chloralose-anesthetized cats. Those effects were blocked by cyproheptadine whereas methysergide potentiated the actions of LSD on visual primary activity. In contrast, LSD depressed the primary somatic pathway, at small doses (25 to 50 micrograms/kg) and facilitated the response at larger doses (200 micrograms/kg). Cyproheptadine and methysergide did not agonize these actions of LSD. The anterior marginal cortex, nucleus central median-parafascicularis, nucleus lateral posterior, and the superior colliculus, all sites of heterosensory convergence, were depressed by LSD. The depression of responses at heterosensory sites by LSD was blocked by cyproheptadine. Methysergide potentiated the LSD-induced depression of visual-evoked activity but not somatosensory activity. These results suggest that LSD depresses sensory activity in regions which integrate multiple sensory modalities independently of actions on sensory-specific pathways. These effects appear to involve a cyproheptadine-sensitive system.

Animals↗
PubMed1983

Blockade of the behavioral effects of lysergic acid diethylamide, 2,5-dimethoxy-4-methylamphetamine, quipazine and lisuride by 5-hydroxytryptamine antagonists.

The effects of lysergic acid diethylamide (LSD), 2,5-dimethoxy-4-methylamphetamine (DOM), quipazine or lisuride alone and in combination with the 5-hydroxytryptamine antagonist metergoline, pizotifen and cinanserin were studied in rats responding on a fixed-ratio 40 schedule of food presentation. LSD, DOM, quipazine or lisuride produced a similar dose-dependent decrease in the number of food presentations (ED50 values: 81 micrograms/kg, 0.6 mg/kg, 1.6 mg/kg and 31 micrograms/kg, respectively) and a reciprocal increase in the number of pause intervals (IRTs = 10 sec). All three antagonists attenuated the behavioral effects of LSD and DOM for both food presentations and pause intervals. The LSD-response curve for reinforcers was shifted to the greatest degree by pizotifen (1.0 mg/kg), followed by cinanserin (20 mg/kg) and metergoline (1.0 mg/kg). The ED50 values for this effect were 334, 181 and 141 micrograms/kg, respectively. The DOM dose-response pattern for decrease in reinforcers was shifted to the greatest degree by metergoline, followed by pizotifen and cinanserin (ED50 values: 26.5, 3.2 and 1.8 mg/kg, respectively). The effect of quipazine on reinforcers was antagonized by metergoline and pizotifen (ED50 values: greater than 8.0 for both) but not by cinanserin, although all three antagonists attenuated the increase in pause intervals in the same order as they did for DOM. The decrease in reinforcers by lisuride was equally antagonized by metergoline and pizotifen (ED50 values: 58 and 57 micrograms/kg, respectively), whereas cinanserin potentiated the effect of lisuride (ED50: 16 micrograms/kg).(ABSTRACT TRUNCATED AT 250 WORDS)

DOM 2,5-Dimethoxy-4-Methylamphetamine↗
PubMed1990

Differentiation between the stimulus effects of (+)-lysergic acid diethylamide and lisuride using a three-choice, drug discrimination procedure.

The discriminative stimulus properties of (+)-lysergic acid diethylamide (LSD) and lisuride hydrogen maleate (LHM), were compared in a three-choice, water reinforced (FR 20) situation in which rats were required to press one lever following LSD (0.08 mg/kg), a second lever following LHM (0.04 mg/kg), and a third lever following saline. Reliable drug-appropriate responding was established in 72 sessions. Dose-response tests with LSD and LHM indicated that, as dose increased, the per cent of responding on the lever associated with the particular training drug also increased; little or no cross-transfer occurred between LSD and LHM. In generalization tests, the serotonin (5-HT) agonist quipazine substituted for LSD but not LHM while the dopamine (DA) agonist apomorphine mimicked LHM but not LSD; an unrelated compound, pentylenetetrazol (PTZ), produced responding on the saline-appropriate lever. In combination tests, 5-HT antagonists (e.g., BC-105 and low doses of pirenperone) blocked responding on the LSD lever while DA antagonists (e.g., haloperidol and much higher doses of pirenperone) blocked LHM-appropriate responding. These data suggest that the three-lever (D-D-N) procedure is similar to, but can be more sensitive than the two-lever (D-N) procedure (because it can differentiate between LSD and LHM); they therefore at least partially support the hypothesis that three-choice discriminations can be conceptualized as two separate, two-choice (D-N) discriminations (Jarbe and Swedberg 1982). The results also confirm suggestion that the stimulus effects of LSD and LHM are mediated by different mechanisms; the primary action of LSD is serotonergic (5-HT2), while that of LHM is dopaminergic (White 1986).

Animals↗
PubMed1993

Lysergic acid diethylamide is a partial agonist at 5-HT2 receptors in ovine uterine artery of late pregnancy.

d-Lysergic acid diethylamide (LSD) produced dose-dependent contractions (EC50, 17.9 +/- 2.1 nM) on isolated ovine uterine artery of late pregnancy, which were competitively antagonized by ketanserin. The maximal contraction to LSD was 51% of the 5-HT response. LSD competitively antagonized (pA2 9.21) contractions produced to 5-hydroxytryptamine (5-HT). The results indicate that LSD is a partial agonist at 5-HT2 receptors in ovine uterine artery.

Animals↗