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PubMed1985

Increased platelet membrane [3H]-LSD binding in patients on chronic neuroleptic treatment.

Using a [3H]-lysergic acid diethylamide [( 3H]-LSD) binding technique, platelet 5-hydroxytryptamine (5-HT) receptor number and affinity were compared in schizophrenics treated with depot thioxanthenes and phenothiazines and controls. There was an approximately 30% increase in platelet receptor number (Bmax) in the patient group. There was a decrease in affinity (increase in Kd) of about 30% in the patient group. This was probably due to the persistence of the neuroleptic in the platelet membrane preparation. There was a weak positive correlation between receptor number and total neuroleptic dosage. The increased number of 5-HT receptors is consistent with the previously reported enhancement of 5-HT-induced platelet aggregation in patients treated with long-term phenothiazines and thioxanthenes. Our findings are compatible with 5-HT up-regulation in human platelets produced by depot neuroleptic therapy. It is not known whether parallel changes may be occurring in brain 5-HT receptors.

Adult↗
PubMed1984

Desensitization of serotonin-stimulated adenylate cyclase in the liver fluke Fasciola hepatica.

Incubation of the intact liver fluke Fasciola hepatica with serotonin (5-HT) resulted in a time-dependent decrease in both 5-HT-stimulated adenylated cyclase activity and specific [3H]LSD binding in the subsequently prepared cell-free fluke particles. In control fluke particles, the activation of adenylate cyclase by 5-HT was biphasic, indicating a high and low affinity form of the 5-HT receptor with half-maximal activation constants (KA) of 0.35 and 2.8 microM respectively. In contrast, 5-HT activation of desensitized particles occurred through a single set of low affinity sites having a KA value of 6.3 microM. The maximal level of 5-HT activation of adenylate cyclase was also reduced in the desensitized particles. Lysergic acid diethylamide (LSD)-stimulated adenylate cyclase activity was also less in the desensitized particles. However, unlike with 5-HT, activation by LSD occurred through a single set of sites for both control and desensitized particles. [3H]LSD binding studies showed that the affinity of LSD for the 5-HT receptors in the control and desensitized particles was similar. Thus, the decrease in [3H]LSD binding and serotonin-stimulated adenylate cyclase activity in the desensitized particles appeared to be due to a preferential loss or inactivation of the high affinity form of the 5-HT receptor. A similar time-dependent loss in 5-HT-stimulated adenylate cyclase and in [3H]LSD binding occurred in cell-free fluke particles upon the addition of 5-HT or LSD. These effects were not due to protein denaturation or metabolism of the ligand during the incubation procedure. This cell-free desensitization was reversible and temperature dependent, and was not affected by ATP or other nucleotides.

Adenosine Triphosphate↗
PubMed1970

Steric and electronic relationships among some hallucinogenic compounds.

Stereochemical considerations and total valence electron calculations suggest congruities among the ostensibly dissimilar hallucinogenic compounds, D-lysergic acid diethylamide (LSD), indolcalkylamines, and methoxylated amphetamines. In LSD the aromatic benzene ring A and the N-6 nitrogen are essential for hallucinogenic activity; these sites may react with the receptor. The conformations of amphetamines and indolealkylamines at the receptor are such that the aromatic benzene ring lies like ring A of LSD and the alkylamino nitrogen lies like the N-6 of LSD. Ring A may interact with the receptor by forming a pi-molecular complex, as suggested by the correlation between hallucinogenic activity and energy of the highest occupied molecular orbital (E(H)) of congeneric series. The N-6 nitrogen of LSD and the sterically congruent nitrogen of the other hallucinogenic compounds may react with the receptor by forming a donor acceptor complex of the n-pi(*) or n-sigma(*) type. Other portions of the hallucinogenic molecules confer a favorable E(H): these include the methoxy and hydroxyl groups of the amphetamines (and mescaline), and the indolealkylamines; and the pyrrole ring of LSD and the indolealkylamines.

Amphetamine↗
PubMed2003

LC-MS analysis of 2-oxo-3-hydroxy LSD from urine using a Speedisk positive-pressure processor with Cerex PolyChrom CLIN II columns.

A rapid and sensitive solid-phase extraction method for the lysergic acid diethylamide (LSD) metabolite 2-oxo-3-hydroxy-LSD (O-H-LSD) was developed for use in a forensic laboratory. The method uses a positive-pressure manifold anion-exchange polymer-based solid-phase extraction with subsequent analysis by liquid chromatography-mass spectrometry (LC-MS). The average extraction efficiency was 92%. The limits of detection (LOD) and quantitation (LOQ) were calculated at 250 pg/mL. The assay was linear, precise, and accurate from 250 to 30,000 pg/mL with an r(2) of 0.999. Samples including 93 compounds with properties similar to O-H-LSD, common over-the-counter products, prescription drugs and some of their metabolites, and other drugs of abuse were analyzed and produced no significant interference. This method has increased our efficiency in analyzing O-H-LSD by reducing the overall extraction and analysis time. The increase in extraction efficiency enabled decreased assay LOD and LOQ values while lowering the volume required for injection.

Equipment Design↗
PubMed1990

Quantitative and autoradiographic analyses of alpha-adrenergic and serotonergic receptors on aorta and coronary artery.

Norepinephrine, epinephrine, and 5-hydroxytryptamine (5-HT) modulate the vascular tone via specific receptors on the vascular wall. Binding characteristics and localization of alpha-adrenergic and serotonergic receptors were determined in porcine aortas and coronary arteries. Radioligand binding studies were done using frozen sections of vascular tissue (10 microns thick), and the obtained data were compared with findings on microsomal fractions prepared from smooth muscle cells. Affinities [dissociation constant (Kd)] of 125I-labeled 2-[beta-(4-hydroxyphenyl)-ethylaminomethyl]-tetralone (BE 2254), an alpha 1-antagonist, for alpha-adrenergic receptors on aortic and coronary microsomal fractions were 190 and 224 pM, respectively. The Kd of 125I-labeled lysergic acid diethylamide (LSD), a serotonergic antagonist, to serotonergic receptors on the aorta was 403 pM, a value less than that obtained for the coronary artery (873 pM, p less than 0.01). The Kd of 125I-BE 2254 on tissue sections from the aorta was 164 pM and did not significantly differ from that obtained for microsomal fractions. Inhibition constants of adrenergic agonists and antagonists for specific 125I-BE 2254 binding on aortic sections were identical with those obtained for microsomal fractions. Receptor densities examined by 125I-BE 2254 and 125I-LSD were higher in the aorta than in the coronary artery. 125I-BE 2254 bound specifically to alpha 1-adrenergic and 125I-LSD to 5-HT1-like receptors. Radiodensities of 125I-BE 2254 and 125I-LSD were homogeneous macroscopically across the aortic media. Silver grains distributed homogeneously over the smooth muscle cells across the media. There was no accumulation of silver grains to the intima.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1990

Modification of serotonergic neuron properties by long-term treatment with serotonin reuptake blockers.

The authors investigated the mechanism of action of the antidepressant serotonin (5-HT) reuptake blocker citalopram in the rat by means of an in vivo electrophysiologic paradigm. In control animals, the acute intravenous administration of citalopram reduced the firing rate of dorsal raphe nucleus serotonergic neurons with an ED50 of 230 micrograms/kg. Rats were treated with citalopram (20 mg/kg/day i.p.) for 2, 7, and 14 days. Two-day treatment was accompanied by a marked reduction of the firing activity of serotonergic neurons; there was a partial recovery after 7 days of treatment, and a complete one following 14-day citalopram administration. The response of serotonergic neurons to intravenously administered lysergic acid diethylamide (LSD), a somatodendritic 5-HT autoreceptor agonist, was reduced in rats treated with citalopram for 14 days, suggesting that such a treatment reduces the sensitivity of the somatodendritic autoreceptor. Fourteen-day citalopram treatment also markedly enhanced the efficacy of the stimulation of the afferent serotonergic pathway in suppressing the firing activity of postsynaptic CA3 dorsal hippocampus pyramidal neurons. This enhanced efficacy of serotonergic synaptic transmission was not the result of an increased sensitivity of postsynaptic neurons to serotonin, as the effect of the direct microiontophoretic application of serotonin onto these same neurons was not modified. That serotonin reuptake blockade per se was responsible for this enhancement could also be ruled out, as the acute intravenous administration of citalopram (1 mg/kg) in control rats failed to enhance the efficacy of the stimulation. To determine an involvement of the 5-HT terminal autoreceptor, methiothepin (1 mg/kg), a terminal autoreceptor antagonist, was injected intravenously in control and citalopram-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Stimulus effects of ibogaine in rats trained with yohimbine, DOM, or LSD.

The stimulus effects of ibogaine were compared with those of yohimbine, an alpha 2-adrenoceptor antagonist, 2,5-dimethoxy-4-methylamphetamine (DOM), a 5-hydroxytryptamine2 (5-HT2) agonist, and lysergic acid diethylamide (LSD), a nonspecific 5-HT agonist. Rats were trained with either yohimbine (6 mg/kg), DOM (0.6 mg/kg), or LSD (0.1 mg/kg) vs. no treatment in a two-lever discrimination task. Tests of generalization were then conducted with ibogaine. In yohimbine-trained animals, 39.7% of responses following ibogaine (15 mg/kg) were on the drug-appropriate lever, but this response level was not significantly different from no treatment-appropriate responding. A response distribution that was significantly different from responding under both drug and no treatment training conditions was observed in DOM-trained rats after administration of 15 mg/kg ibogaine. Pizotyline (BC-105) blocked all DOM-appropriate responding produced by ibogaine. In LSD-trained animals, 20 mg/kg ibogaine mimicked LSD. Pizotyline blocked LSD-appropriate responding produced by ibogaine in five of six animals. The present data suggest the involvement of 5-HT2 receptor activity, and the possibility of a 5-HT1A contribution, in the stimulus properties of ibogaine.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗
PubMed1997

Determination of LSD in blood by capillary electrophoresis with laser-induced fluorescence detection.

Capillary electrophoresis (CE) with HeCd laser-induced fluorescence (LIF) detection and its application in forensic toxicology is demonstrated by the determination of D-lysergic acid diethylamide (LSD) in blood. Following precipitation of proteins, washing of the evaporated supernatant and extraction, the residue was reconstituted in methanol and injected electrokinetically (10 s, 10 kV). The total analysis time for quantification of LSD was 8 min using a citrate-methanol buffer, pH 4.0. With this buffer system it is possible to separate LSD, nor-LSD, iso-LSD and iso-nor-LSD. Using a specific sample preparation, electrokinetic injection, extended light path (bubble cell) capillaries and especially LIF detection (lambda(ex) 325 nm, lambda(em) 435 nm), a limit of detection of 0.1-0.2 ng LSD per ml blood could be obtained. The limit of quantitation was about 0.4-0.5 ng/ml. The quantitative evaluation for LSD was carried out using methylergometrine as internal standard. The precision expressed as coefficient of variation (C.V.) and accuracy of the method were <20% and 86-110%, respectively. The application of the method to human blood samples from two forensic cases and a comparison with radioimmunoassay demonstrated that the results were consistent.

Electrophoresis, Capillary↗
PubMed2002

Flashback and Hallucinogen Persisting Perception Disorder: clinical aspects and pharmacological treatment approach.

One unique characteristic of lysergic acid diethylamide (LSD) and LSD-like substances is the recurrence of some of the symptoms which appeared during the intoxication after the immediate effect of the hallucinogen has worn off. This recurring syndrome, mainly visual, has not been clearly understood, appreciated or distinguished from other clinical entities by clinicians. The terms Flashback and Hallucinogen Persisting Perception Disorder (HPPD) are used interchangeably in the professional literature. Flashback is a usually short-term, non-distressing, spontaneous, recurrent, reversible and benign condition accompanied by a pleasant affect. In contrast, HPPD is a generally long-term, distressing, spontaneous, recurrent, pervasive, either slowly reversible or irreversible, non-benign condition accompanied by an unpleasant dysphoric affect. Flashback and HPPD appear to be part of a vast and broad spectrum of non-psychopathological and psychopathological states reported by hallucinogen users. Pharmacological agents such as clonidine, perphenazine and clonazepan have been shown to ameliorate this syndrome in some of the individuals seeking treatment.

Clonazepam↗
PubMed1989

Serotonin receptors in the tissues of adult Ascaris suum.

Serotonin (5-hydroxytryptamine, 5-HT) receptors in the muscle and intestinal tissues of adult Ascaris suum have been investigated. [3H] lysergic acid diethylamide (LSD) exhibited specific and saturable binding to membranes prepared from both intestine and muscle. The intestinal tissue membranes had an equilibrium dissociation constant (Kd) of 2.70 nM for LSD and a Kd of 2.50 microM for 5-HT. As compared to the intestine, the muscle membranes had comparatively higher affinity for both LSD (Kd = 1.80 nM) and 5-HT (Kd = 0.68 microM). The muscle membranes also had a high binding affinity for ketanserin, a 5-HT2 antagonist, (Kd = 16.7 nM) whereas intestinal membranes exhibited no specific binding of ketanserin. Serotonin significantly inhibited the binding of LSD to the intestinal and muscle tissue membranes while adrenergic and cholinergic drugs and histamine did not. This suggested that the binding of LSD, 5-HT and ketanserin to the parasite membranes was specific. Collectively, the data demonstrated the presence of a serotonin receptor in the muscle and intestinal tissues of the adult A. suum. The receptor in the muscle was pharmacologically similar to the mammalian serotonin type 2 receptor.

Animals↗
PubMed1982

Analyzing mechanism(s) of hallucinogenic drug action with drug discrimination procedures.

Some of the advantages of using drug discrimination (DD) procedure to analyze the mechanisms of action of hallucinogenic and related drugs were illustrated by reviewing research with lysergic acid diethylamide (LSD). Because they ensure that drug-induced alterations in interoceptive "state" become biologically meaningful "cues," these procedures are reliable, robust, sensitive and specific. With reference to LSD, many DD experiments suggest: (1) that while hallucinogens substitute for (mimic) LSD (in rats), such substitution does not predict hallucinogenic potency (in humans) but does predict similarities in mechanism(s) of action; (2) the behavioral (in vivo) effects of LSD, unlike those of some of its congeners, are mediated primarily by central, serotonergic (5-HT) neuronal mechanism although LSD may also have (secondary) dopamine (DA) agonist properties; (3) both the locus and the nature of these LSD-5-HT interactions are unclear: cells arising from B-7, B-8 and B-9 regions of the dorsal-medial raphe may be involved; pretreatment with agents that deplete 5-HT and increase the stereospecific binding of 3H-LSD in vitro (p-chlorophenylalanine; 5,7-dihydroxytryptamine) enhance sensitivity to LSD in vivo.

Animals↗
PubMed2005

Development of homogeneous high-affinity agonist binding assays for 5-HT2 receptor subtypes.

The serotonin (5-hydroxytryptamine) 5-HT2 receptor subfamily consists of three members, 5-HT2A, 5-HT2B, and 5-HT2C. These receptors share high homology in their amino acid sequence, have similar signaling pathways, and have been indicated to play important roles in feeding, anxiety, aggression, sexual behavior, mood, and pain. Subtype-selective agonists and antagonists have been explored as drugs for hypertension, Parkinson's disease, sleep disorders, anxiety, depression, schizophrenia, and obesity. In this study, we report the development of homogeneous agonist binding assays in a scintillation proximity assay (SPA) format to determine the high-affinity binding state of agonist compounds for the human 5-HT2C, 5-HT2A, and 5-HT2B receptors. The 5-HT2 agonist 1-(4- [125I]iodo-2,5-dimethoxyphenyl)-2-aminopropane ([125I]DOI) was used to label the high-affinity sites for the 5-HT2A and 5-HT2C receptors. The high-affinity sites for the 5-HT2B receptor were labeled with [3H]lysergic acid diethylamide. Total receptor expression was determined with the 5-HT2 antagonist [3H]mesulergine for the 5-HT2B and 5-HT2C receptors, and [3H]ketanserin for the 5-HT2A receptor. The agonist high-affinity binding sites accounted for 2.3% (5-HT(2C) receptor), 4.0% (5-HT2A receptor), and 22% (5-HT2B receptor) of the total receptor population. Competition binding studies using known agonists indicated high Z' values of the agonist binding assays in SPA format (Z' > 0.70). The Ki values of 5-HT, (R)(-)DOI, and VER-3323 for the 5-HT2A, 5-HT2B, and 5-HT2C receptors by SPA format were equivalent to published data determined by filtration binding assays. These results indicate that agonist binding assays in SPA format can be easily adapted to a high throughput assay to screen for selective 5-HT2C receptor agonists, as well as for selectivity profiling of the compounds.

Amphetamines↗
PubMedDate not supplied

The development and application of a gas chromatography-mass spectrometric (GC-MS) assay to determine the presence of 2-oxo-3-hydroxy-LSD in urine.

An accurate and reproducible gas chromatography-mass spectrometry (GC-MS) analytical method was developed to enable the Laboratory to determine the presence and concentration of the 2-oxo-3-hydroxy metabolite of lysergic acid diethylamide (OH-LSD) in urine. The limit of detection was 0.5 ng/mL, with a limit of quantitation established as 1.0 ng/mL. The assay was reproducible and linear over the concentration range 0.5-50.0 ng/mL, with a typical correlation coefficient (r2) of 0.997. This method was subsequently applied to the analysis of specimens submitted for routine drugs of abuse screening as part of an audit into the prevalence of LSD abuse in the West Midlands, U.K. This initial pilot study was performed using urine specimens obtained from 600 suspected LSD abusers. Following immunoassay screening, only 25 (6 female and 19 male subjects) were found to be LSD positive, but only 11 were confirmed as containing OH-LSD by GC-MS. The concentrations determined in these specimens ranged from 1.7 to 55.8 ng/mL (mean 11.0, median 5.4). This rapid and sensitive technique should enable the Laboratory to perform future audits of LSD abuse throughout the West Midlands and facilitate differential diagnoses to be made between drug misuse and underlying organic disorders.

Administration, Oral↗
PubMed1989

Hallucinogenic drug interactions with neurotransmitter receptor binding sites in human cortex.

The binding affinities of four hallucinogenic agents were analyzed at nine neurotransmitter binding sites in human cortex. d-Lysergic acid diethylamide (d-LSD), N,N-dimethyltryptamine (DMT), 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) and 1-(2,5-dimethoxy-4-bromophenyl)-2-aminopropane (DOB) display highest affinity for the recently identified "DOB binding site" labeled by 77Br-R(-)DOB. The phenalkylamines, DOI and DOB, display subnanomolar affinity for the 77Br-R(-)DOB-labeled site, whereas the indolealkylamines, d-LSD and DMT, display nanomolar affinity for this site. d-LSD was the most potent of the four hallucinogens at six of the other eight sites analyzed in this study. All four hallucinogens also display high affinity for the 5-hydroxytryptamine2 (5-HT2) receptor subtype, with potencies ranging from 4 to 360 nM. Marked differences in relative affinities were observed between the indolealkylamines and the phenalkylamines at the 5-HT1A, 5-HT1D, and DOB binding sites. These rank-order differences in affinities are likely to account for the differing effects of these agents in various biochemical and physiological assays.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗
PubMed1981

Effects of selected opioid agonists and antagonists on DMT- and LSD-25-induced disruption of food-rewarded bar pressing behavior in the rat.

Several opioid agonists and antagonists interact with N,N-dimethyltryptamine (DMT) and lysergic acid diethylamide-25 (LSD) in adult male Holtzman rats trained on a positive reinforcement, fixed ratio 4 (FR4) behavioral schedule, i.e., a reward of 0.01 ml sugar-sweetened milk was earned on every fourth bar press. DMT (3.2 and 10.0 mg/kg) and LSD (0.1 mg/kg) given IP with 0.9% NaCl pretreatment, disrupted food-rewarded FR4 bar pressing. Animals were pretreated IP (10--15 min) with predetermined, behaviorally noneffective doses of morphine, methadone, naltrexone, and the (+)- and (-)-enantiomers of naloxone prior to receiving DMT or LSD. Dose-dependent effects were shown with opioid agonist pretreatment. Morphine (0.32--1.0 mg/kg) and methadone (0.32 mg/kg) significantly antagonized the bar pressing disruption induced by DMT and LSD. Larger doses of morphine (3.2 mg/kg) and methadone (1.0--3.2 mg/kg) potentiated only LSD-induced effects, with no effect on DMT-treated groups. The opioid antagonists (-)-naloxone and naltrexone potentiated the disruption of bar pressing induced by DMT and LSD. Failure of (+)-naloxone to potentiate the DMT effects was attributed to a stereo-specific opioid antagonist effect of (-)-naloxone.

Animals↗
PubMed1979

Naloxone enhancement of DMT and LSD-25 induced suppression of food-rewarded bar pressing behavior in the rat.

The narcotic antagonist naloxone was tested to determine its possible interaction with N,N-dimethyltryptamine (DMT) and lysergic acid diethylamide-25 (LSD) in adult male Holtzman rats trained to press a bar on a fixed-ratio four schedule (FR4), i.e., every fourth press earned a reward of 0.01 ml sugar sweetened milk. LSD (0.1 mg/kg) or increasing doses of DMT (1.0, 3.2, and 10.0 mg/kg) were administered i.p. to disrupt food-rewarded fixed ratio bar pressing in a dose related fashion. Pretreatment (5--10 min) with behaviorally ineffective doses of naloxone (1.0--5.6 mg/kg) dramatically enhanced the effects of DMT and LSD. The content of DMT in the brain and liver of rats injected with DMT alone (10 mg/kg) and with a 5 min pretreatment of naloxone (3.2 mg/kg) was determined by radiochemical analysis at 30 and 90 min after 14C-DMT injection. There was no significant difference for either brain or liver 14C-DMT levels when control DMT rats were compared with the naloxone pretreated rats. These results seem to rule out interference by naloxone with the metabolism of DMT as a mechanism of the observed behavioral potentiation.

Animals↗
PubMed1999

Enhanced platelet serotonin 5-HT2A receptor binding in anorexia nervosa and bulimia nervosa.

Some evidence exists to suggest that serotonin 5-HT2A receptor function is altered in anorexia nervosa and bulimia nervosa. In order to further investigate the 5-HT2A receptor in eating disorders, platelet [3H]lysergic acid diethylamide ([3H]LSD) binding was studied in ten patients with anorexia nervosa, 23 patients with bulimia nervosa and 33 healthy controls. At admission, Bmax for platelet [3H]LSD binding was significantly higher both in the anorexia nervosa group (30.6+/-4.2 fmol/mg protein; mean+/-S.D.) and in the bulimia nervosa group (30.8+/-7.6 fmol/mg protein) than in the control group (23.5+/-6.3 fmol/mg protein; p=0.01 and p=0.003, respectively). Kd was borderline significantly higher among anorexics (median 1.45 nM) and significantly higher among bulimics (median 1.66 nM) than among controls (median 0.95 nM; p=0.05 and 0.003, respectively). The Global Assessment of Functioning score and the body mass index were both significantly negatively correlated to Kd (r=-0.40; p=0.03 and r=-0.41 p=0.03, respectively), but not to Bmax. The present study indicates that patients with anorexia nervosa as well as patients with bulimia nervosa have an enhanced 5-HT2A receptor binding and provides further evidence for a serotonergic dysfunction in eating disorders.

Adolescent↗
PubMed1997

The effect of fluvoxamine on serum prolactin and serum sodium concentrations: relation to platelet 5-HT2A receptor status.

Hyperprolactinemia and hyponatremia are adverse drug reactions regularly reported for selective serotonin reuptake inhibitors. Results from animal studies suggest that serotonin receptors of different subtypes are involved in the mediation of these effects. We have investigated to what extent fluvoxamine alters serum prolactin and serum sodium levels and whether these effects are related to platelet 5-hydroxytryptamine 2A (5-HT2A) receptor status, as studied by [3H]lysergic acid diethylamide ([3H]LSD) binding. Eight healthy subjects were given fluvoxamine in increasing dosage from 25 mg/day to 200 mg/day during 4 weeks, and serum sodium and serum prolactin concentrations were obtained weekly. All subjects had normal prolactin and sodium levels before start of treatment. Two subjects had substantial increases in serum prolactin levels (up to 35 microg/L) during fluvoxamine treatment, and these two subjects had higher Bmax for platelet [3H]LSD binding before fluvoxamine treatment than the six other subjects (32.7 vs. 23.1 fmol/mg protein). There was a small, nonsignificant decrease (mean 1.0 mmol/L) in serum sodium levels after institution of fluvoxamine but a significant increase (mean 1.9 mmol/L) in serum sodium levels after discontinuation of the drug (p = 0.02). Bmax for [3H]LSD binding and change in serum sodium concentration after institution of fluvoxamine showed a significant positive correlation (r = 0.85;p = 0.007). The results indicate that fluvoxamine affects serum prolactin as well as serum sodium concentrations and lend indirect support to the suggestion that 5-HT2A receptors might be involved in the mediation of these effects.

Adult↗