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At least 847 records · Page 47Linked to original sources
PubMed1970

Some factors influencing the release of 5-hydroxyindol-3-ylacetic acid in the forebrain.

1. Electrical stimulation of the mid-brain raphé in anaesthetized adrenalectomized rats produced a significant decrease in the forebrain content of 5-hydroxytryptamine (5-HT) and an increase in the concentration of 5-hydroxyindol-3-ylacetic acid (5-HIAA).2. Stimulation of peripheral sensory nerves did not influence either the forebrain content of 5-HIAA or the efflux of 5-HIAA from the cerebral cortex.3. Probenecid (200 mg/kg) caused a twofold increase in 5-HIAA content of the rat's forebrain, while the efflux of 5-HIAA from the cerebral cortex remained unchanged.4. Stimulation of the mid-brain raphé in animals pretreated with probenecid does not produce the rise in the forebrain levels of 5-HIAA seen in stimulated untreated controls and does not affect the efflux of 5-HIAA from the cerebral cortex.5. In preliminary experiments, lysergic acid diethylamide (LSD 25) substantially reduced and/or prevented the increase in the release of 5-HIAA in the forebrain observed in untreated animals with raphé stimulation.

Adrenalectomy↗
PubMed1984

Cardiovascular changes produced by the injection of aconitine at the area of the locus coeruleus in unanesthetized rats.

Blood pressure, heart rate and electrocardiogram were monitored in unanesthetized, unrestrained rats while the area of the locus coeruleus was stimulated by the injection of 0.03 to 10 micrograms of aconitine to pharmacologically evaluate its cardiovascular action. Aconitine elicited a dose-dependent elevation of mean blood pressure to 200 mmHg; at doses of 1-10 micrograms, it increased heart rate by more than 100 beats/min and produced arrhythmias. Phentolamine and the serotonergic antagonist, 2-bromo-lysergic acid diethylamide, prevented aconitine-induced cardiovascular changes. Diminution of aconitine-induced tachycardia by propranolol was attributed to the antagonist's direct peripheral effects. Atropine (5 mg/kg, subcutaneously) did not alter aconitine's cardiovascular actions. It is suggested that stimulation of the area of the locus coeruleus with aconitine elicits specific cardiovascular effects, which may involve adrenergic as well as serotonergic pathways.

Aconitine↗
PubMed1978

Blockade of photically induced epilepsy by 'dopamine agonist' ergot alkaloids.

The effect of the intravenous administration of ergot alkaloids on epileptic responses to intermittent photic stimulation )IPS) has been studied in adolescent baboons, Papio papio, from Senegal. Ergocornine, 1--2 mg/kg, produced marked autonomic and behavioural effects, slowed the EEG, and abolished myoclonic responses to IPS for 30--90 min. Ergometrine, 1 mg/kg, activated the EEG and blocked the induction of myoclonic responses for 1--3 h. Bromocriptine, 0.5--4 mg/kg, did not consistently prevent myoclonic responses to IPS. After pretreatment with a subconvulsant dose of allylglycine (180--200 mg/kg), lysergic acid diethylamide, 0.1 mg/kg, retained the capacity to block myoclonic responses to IPS, and ergocornine 1 mg/kg reduced such responses. The convulsant effect of allylglycine was enhanced, however, so that prolonged seizure sequences began 19--96 min after ergocornine administration. The protective action of ergot alkaloids against epileptic responses induced by sensory stimulation is interpreted in terms of effects at several sites, including dopaminergic and serotoninergic synapses.

Allyl Compounds↗
PubMed1982

A chronic impairment of colour vision in users of LSD.

Forty-six users of the hallucinogen lysergic acid diethylamide were compared with 31 controls on a test of colour discrimination an average of two years after their last exposure to the drug. Controls performed better than users, and LSD users without flashbacks performed better than users with flashbacks. An analysis of variance between the three groups was significant at P less than 0.001. This study suggests that some users of LSD may have a sustained or irreversible impairment in colour discrimination.

Adolescent↗
PubMed1978

Inhibition of compound 48/80-induced intradental sensory nerve activity by disodium cromoglycate and serotonin antagonists.

Local application of compound 48/80 induced long lasting nerve activity in intradental sensory nerves in the teeth of cats and dogs. This effect was inhibited by pretreatment with disodium cromoglycate (DSCG) given locally (2 X 10(-2) M) or i.a. (20 mg/min). DSCG did not have any effect on the nerve excitability per se, as judged from the responses to hypertonic NaCl and air blasta applied to exposed dentin before and after administration of DSCG. Local treatment with lysergic acid diethylamide (0.1--1 mg/ml) and methysergide (0.05--0.5 mg/ml) selectively reduced or inhibited the compound 48/80 induced nerve activity. Systemic administration of methysergide (12.5 microgram/kg) prevented the excitatory effects of compound 48/80 but was without effect when administrated during a state of established activity. The present findings support the hypothesis that compound 48/80 has an indirect effect on intradental sensory nerves and indicate that vascular reactions take part in intradental sensory nerve excitation.

Action Potentials↗
PubMed1998

Second thoughts on psychedelic drugs.

Psychedelic drugs are making a comeback. Proponents of psychedelics point to the widespread medical experimentation with mescaline and lysergic acid diethylamide-125 (LSD) in the 1950s as proof of their safety and efficacy. However, a review of the private and published writings of Sidney Cohen, MD, who conducted the first study of the safety of psychedelics, reveals that serious medical concerns about psychedelics arose before the public backlash against the drugs in the 1960s. The story of psychedelic research is a reminder of the inevitable complications involved in testing drugs on human subjects.

Drug Approval↗
PubMed1996

LSD-like panic from risperidone in post-LSD visual disorder.

Risperidone, a novel antipsychotic agent, is an antagonist of postsynaptic serotonin-2 and dopamine D2 receptors. In certain individuals, the hallucinogenic drug lysergic acid diethylamide (LSD) is associated with apparently lifelong continuous visual disturbances, characterized in DSM-IV as hallucinogen-persisting perception disorder (HPPD). Because the hallucinogenic mechanism of LSD is known to act in part at postsynaptic serotonin-2 receptors, it is noteworthy that three HPPD patients treated with risperidone reported an exacerbation of LSD-like panic and visual symptoms. We conclude that HPPD may be a relative contraindication for the use of risperidone.

Adult↗
PubMed1970

LSD: no teratogenic action in rats, mice, and hamsters.

Lysergic acid diethylamide tartrate was given to 98 pregnant rats, 67 mice, and 22 hamsters as a single dose of 5 to 500 micrograms per kilogram of body weight per day either at the beginning of gestation or during the period of organogenesis. Examination of the 1003 rat fetuses, 521 mouse fetuses, and 189 hamster fetuses obtained failed to prove any abortifacient, teratogenic, or growth-depressing effects.

Abnormalities, Drug-Induced↗
PubMed1980

Monoamine replacement after reserpine: catecholaminergic agonists restore motor activity but phenylethylamine restores atropine-resistant neocortical low voltage fast activity.

A large dose of reserpine abolishes an atropine-resistant form of neocortical low voltage fast activity (LVFA) which normally accompanies certain patterns of motor activity in rats. An attempt was made to reverse this effect by replacement of specific monoamines or by injection of suitable agonists in rats pretreated with reserpine (10 mg/kg). The following compounds, alone or in various combinations, failed to restore atropine-resistant LVFA in reserpinized rats even though spontaneous motor activity was restored in many cases: L-DOPA (150-300 mg/kg) after pretreatment with an inhibitor of peripheral L-aromatic amino acid decarboxylase; 5-hydroxytryptophan (100-200 mg/kg); D-amphetamine (1-2 mg/kg); apomorphine (0.25-2.5 mg/kg); lysergic acid diethylamide (100-300 microgram/kg); and clonidine (0.5-1.0 mg/kg). In contrast beta-phenylethylamine was quite effective in restoring atropine-resistant LVFA and its effects were not diminished by pretreatment with alpha-methyl-p-tyrosine (400 mg/kg), chlorpromazine (15 mg/kg). It is suggested that a trace amine plays an essential role in the production of atropine-resistant LVFA independent of catecholamines.

5-Hydroxytryptophan↗
PubMed1985

Microchemical synthesis of the serotonin receptor ligand, 125I-LSD.

The synthesis and properties of 2-[125I]-lysergic acid diethylamide, the first 125I-labeled serotonin receptor ligand, are described. A novel microsynthesis apparatus was developed for this synthesis. The apparatus employs a micromanipulator and glass micro tools to handle microliter to nanoliter volumes on a microscope stage. This apparatus should be generally useful for the synthesis of radioligands and other compounds when limited amounts of material must be handled in small volumes.

Animals↗
PubMed1977

An analysis of the anatomical basis for the mechanical response to motor nerve stimulation of the rat vas deferens.

1. An anatomical basis was sought for the biphasic motor nerve response of the rat vas deferens. The motor nerve pathway to the tissue was stimulated at different points between the vertebral outflow and the intramural fibres, in the pithed rat and in isolated tissues, to examine the possibility of two anatomically separate groups of neurones. Different preparations of the isolated tissue were devised to detect whether different groups of smooth muscle fibres contributed to the two phases.2. The fibres mediating both phases of the response arose from the upper lumbar vertebral outflows. Both phases were elicited by pre- or post-ganglionic stimulation and could be depressed by hexamethonium. In the pithed rat or with hypogastric nerve stimulation in the isolated tissue, however, the initial ;twitch' phase was relatively resistant to such blockade.3. When the rat vas deferens was perfused through the lumen in situ or in vitro, the perfusion pressure response to motor nerve stimulation exhibited two phases similar to those of the longitudinal contractile response.4. Isolated rat vasa were bisected into portions, each of which was stimulated and longitudinal tension was recorded. The proportions of the two phases of the response varied along the length of the tissue. At the prostatic end the total response was relatively weak with a dominant ;twitch' and at the epididymal end the two phases were comparable in magnitude. The distribution of adrenergic nerve terminals within the muscle layers also varied along the length of the rat vas deferens.5. The effects of drugs were investigated on the motor responses of the above preparations. The ;twitch' phase was relatively susceptible to blockade by reserpine and lysergic acid diethylamide and the ;secondary' phase to phentolamine with both equally sensitive to guanethidine. Each phase had similar susceptibilities to blockade irrespective of which part of the tissue was involved.6. It was concluded that two types of nerve-muscle transmission may be involved in the rat vas deferens with the proportion of each varying along the length of the tissue but both displaying pharmacological characteristics of adrenergic fibres.

Adrenergic Fibers↗
PubMed1959

Mechanism of action of reserpine in producing gastric haemorrhage and erosion in the mouse.

Gastric haemorrhage was produced regularly in mice within 6 hours of the subcutaneous injection of a large dose (2 to 10 mg./kg.) of reserpine or of deserpidine. Rescinnamine, syrosingopine (SU-3118), and tetrabenazine (Ro 1-9569) were less active. Gastric haemorrhage was also produced within 6 hours when 5-hydroxytryptamine (10 mg./kg.) was injected every half-hour. Neither reserpine nor 5-hydroxytryptamine produced gastric haemorrhage in mice which had been vagotomized by tying the oesophagus at the cardio-oesophageal junction or which had been pre-treated with iproniazid. Amphetamine was less effective than iproniazid in preventing gastric haemorrhage after reserpine, and the following drugs were ineffective: cocaine, methyl phenidate (Ritalin), amarin, caffeine, nikethamide, lysergic acid diethylamide and its 2-bromo derivative (BOL148). Gastric haemorrhage was not observed in mice which had been given substantial doses of atropine or of hexamethonium before reserpine. The incidence of haemorrhage was substantially reduced by treatment with an antacid mixture. It is concluded that reserpine-like drugs cause gastric haemorrhage by a mechanism which has an important central component and which involves the liberation of 5-hydroxytryptamine.

Amphetamine↗
PubMed1976

Effects of drugs acting on cerebral 5-hydroxytryptamine mechanisms on dopamine-dependent turning behaviour in mice.

1. The effects of drugs acting on cerebral 5-hydroxytryptaminergic mechanisms on drug-induced turning behaviour in mice with unilateral destruction of nigro-striatal dopaminergic nerve terminals have been studied. 2. Administration of L-tryptophan (400 mg/kg) or 5-hydroxytryptophan (200 mg/kg) increased brain 5-hydroxytryptamine and decreased the turning induced by both apomorphine (2 mg/kg) and amphetamine (5 mg/kg). 3. Parachlorophenylalanine (3 X 500 mg/kg) decreased brain 5-hydroxytryptamine and increased both apomorphine and amphetamine-induced circling behaviour. 4. Varying the protein content of dietary intake significantly altered brain 5-hydroxytryptamine and tryptophan levels, spontaneous locomotor activity and amphetamine-induced circling behaviour in these mice. 5. Systemic administration of methysergide (0.5-4 mg/kg), lysergic acid diethylamide (0.025-0.2 mg/kg), cyproheptadine (2.5-20 mg/kg) or clomipramine (0.6-20 mg/kg) produced no consistent effect on drug-induced turning behaviour. 6. The results suggest that circling behaviour due to striatal dopamine receptor stimulation is depressed by an elevation of brain 5-hydroxytryptamine and enhanced by a reduction in brain 5-hydroxytryptamine. 7. The possible physiological relationship between dopamine and 5-hydroxytryptamine neurones in the basal ganglia is discussed.

Amphetamines↗
PubMed1978

Adrenergic and 'non-adrenergic' components in the contractile response of the vas deferens to a single indirect stimulus.

1. The mechanical response of the longitudinal smooth muscle of the rat vas deferens to stimulation of its motor nerves by a single pulse has been examined. The motor nerves were stimulated in vivo via the spinal outflows in the pithed rat or in vitro by field stimulation. 2. The contraction in the whole vas consisted of two components, an initial, rapid, brief contraction reaching a maximum at 300 msec and a second, slower and more prolonged contraction reaching its maximum at 600 msec. When the isolated vas was divided into prostatic and epididymal halves the contribution of these two components varied. The initial rapid component was more prominent in the prostatic half and the slower, second component more prominent in the epididymal half. Lowering the bath temperature caused, in both halves, these two components to merge into a single, slow, prolonged response. Both components were more rapid and briefer than the equivalent response of rat anococcygeus. 3. The second, slow component was abolished by alpha-adrenoceptor antagonist drugs, potentiated and prolonged by drugs which inhibit the neuronal uptake of noradrenaline and absent from tissues taken from rats pre-treated with reserpine, suggesting that the neurotransmitter for this component is noradrenaline. 4. These experiments were extended to the mouse or guinea-pig vas deferens. Both showed the same two component mechanical response as the rat vas and in both the second, slow component was preferentially inhibited by alpha-adrenoceptor antagonists and potentiated by drugs blocking noradrenaline uptake. 5. Drugs known to reduce the response to repetitive nerve stimulation of the vas were examined for their effect on the response to a single stimulus. Lysergic acid diethylamide preferentially inhibited the second, slow phase of contraction whereas apomorphine preferentially inhibited the first rapid phase. Guanethidine inhibited responses but any differential effects could not be analysed due to its stimulant properties. 6. These results show that there are two components even to the response to a single stimulus. The second of these appears to be adrenergic while the transmitter responsible for the first remains to be determined.

Adrenergic Fibers↗
PubMed1983

The effects of drugs on the discrimination of color following a variable delay period: a signal detection analysis.

Six pigeons were trained in a chamber with three response keys. Following an observing response on the center key, either colored or noncolored (white) lights were projected on that key. A second center key observing response provided an opportunity to respond on one of the side keys, appropriate to the stimuli presented, to obtain food; responding on the incorrect side produced a 30-s time-out. A delay period of varying duration with no stimuli followed stimulus presentation; the length of the delay was determined 'on-line', such that performance would be maintained at about 80% correct. Lysergic acid diethylamide (LSD, 0.04-0.2 mg/kg) had no significant effect on the accuracy of the discrimination (overall percent correct responses), even at doses that produced cessation of responding in some animals. Amphetamine (1-4 mg/kg) and morphine (0.5-4 mg/kg) decreased accuracy by decreasing sensitivity (A') and had little effect on reaction time. Haloperidol (0.5-2 mg/kg) had no significant effect on any measure of performance. None of the drugs altered response bias (B").

Amphetamine↗
PubMed1979

Dissociations between the effects of LSD on behavior and raphe unit activity in freely moving cats.

The hypothesis that the action of hallucinogenic drugs is mediated by a depression of the activity of brain serotonergic (raphe) neurons was tested by examining the behavioral effects of d-lysergic acid diethylamide (LSD) while studying the activity of raphe neurons in freely moving cats. Although the results provide general support for the hypothesis, there were several important dissociations. (i) Low doses of LSD produced only small decreases in raphe unit activity but significant behavoiral changes; (ii) LSD-induced behavioral changes outlasted the depression of raphe unit activity; and (iii) raphe neurons were at least as responsive to LSD during tolerance as they were in the nontolerant condition.

Animals↗
PubMedDate not supplied

LC-mS analysis of human urine specimens for 2-oxo-3-hydroxy LSD: method validation for potential interferants and stability study of 2-oxo-3-hydroxy LSD under various storage conditions.

2-Oxo-3-hydroxy lysergic acid diethylamide (O-H-LSD), a major LSD metabolite, has previously been demonstrated to be a superior marker for identifying LSD use compared with the parent drug, LSD. Specifically, O-H-LSD analyzed using liquid chromatography-mass spectrometry has been reported to be present in urine at concentrations 16 to 43 times greater than LSD. To further support forensic application of this procedure, the specificity of the assay was assessed using compounds that have structural and chemical properties similar to O-H-LSD, common over-the-counter products, prescription drugs and some of their metabolites, and other drugs of abuse. Of the wide range of compounds studied, none were found to interfere with the detection of O-H-LSD or the internal standard 2-oxo-3-hydroxy lysergic acid methyl propylamide. The stability of O-H-LSD was investigated from 0 to 9 days at various temperatures, pH conditions, and exposures to fluorescent light. Additionally, the effect of long-term frozen storage and pH was investigated from 0 to 60 days. There was no significant loss of O-H-LSD under both refrigerated and frozen conditions within the normal human physiological pH range of urine (4.6-8.4). However, significant loss of O-H-LSD was observed in samples prepared at pH 4.6-8.4 and stored at room temperature or higher (24-50 degrees C).

Biomarkers↗
PubMed1981

Long-term treatment with zimelidine leads to a reduction in 5-hydroxytryptamine neurotransmission within the central nervous system of the mouse and rat.

Male rats and mice received a 14 day peroral treatment with zimelidine, a novel antidepressant drug. Zimelidine produced a 70 and 60% reduction in the number of high affinity [3H]5-hydroxytryptamine (5-HT) and [3H]D-lysergic acid diethylamide (LSD) binding sites, respectively, and induced low affinity binding sites for [3H]5-HT and for [3H]D-LSD. The head twitch behaviour induced by 5-hydroxytryptophan and 5-methoxydimethyltryptamine was attenuated and reductions of prolactin and growth hormone were observed. These findings give further evidence that long-term treatment with zimelidine can produce a reduction of 5-HT neurotransmission in several brain regions.

Animals↗