Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LYSERGIC ACID DIETHYLAMIDE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,297 records · Page 72Linked to original sources

[Hallucinogenic mushrooms].

The group of hallucinogenic mushrooms (species of the genera Conocybe, Gymnopilus, Panaeolus, Pluteus, Psilocybe, and Stropharia) is psilocybin-containing mushrooms. These "magic", psychoactive fungi have the serotonergic hallucinogen psilocybin. Toxicity of these mushrooms is substantial because of the popularity of hallucinogens. Psilocybin and its active metabolite psilocin are similar to lysergic acid diethylamide. These hallucinogens affect the central nervous system rapidly (within 0.5-1 hour after ingestion), producing ataxia, hyperkinesis, and hallucinations. In this review article there are discussed about history of use of hallucinogenic mushrooms and epidemiology; pharmacology, pharmacodynamics, somatic effects and pharmacokinetics of psilocybin, the clinical effects of psilocybin and psilocin, signs and symptoms of ingestion of hallucinogenic mushrooms, treatment and prognosis.

Adolescent↗

5-hydroxytryptamine (HT)1A receptors and the tail-flick response. II. High efficacy 5-HT1A agonists attenuate morphine-induced antinociception in mice in a competitive-like manner.

This study examined the influence of s.c. administration of 5-hydroxytryptamine (HT)1A agonists upon the antinociceptive action of s.c. injected morphine in tail-flick tests to noxious heat and pressure. The selective 5-HT1A agonist, (+-)-8-hydroxy-diprolaminotetralin HBr (8-OH-DPAT), dose-dependently antagonized morphine-induced antinociception (MIA) without affecting the latency to respond when applied alone. In the presence of increasing doses of 8-OH-DPAT (0.16-0.63 mg/kg), the morphine dose-response curve was shifted progressively in parallel to the right and the maximal effect of morphine was not altered; Schild analysis yielded a slope of close to -1.0. 8-OH-DPAT both prevented and reversed the action of morphine. The action of 8-OH-DPAT was reversible (at 24 hr). In distinction, 8-OH-DPAT neither blocked morphine-induced Straub tail nor precipitated withdrawal in morphine-dependent animals; thus, it lacked opioid-antagonist properties. The antagonism of MIA by 8-OH-DPAT was mimicked by additional drugs acting as high efficacy 5-HT1A agonists: lisuride, 5-methoxy-N,N-dimethyltryptamine hydrogen oxalate, RU 24969 [methoxy-3-(1,2,3.6-tetrahydropyridin-4-yl)-1H-indole] and d-lysergic acid diethylamide. In contrast, the 5-HT1B/1C agonist, TFMPP m-trifluromethylphenylpiperazine HCl, and the 5-HT1C/2 agonist, DOI (+-)-2,5-dimethoxy-4-iodophenyl-2-aminopropane HCI, were ineffective. The putative selective 5-HT1A antagonists, BMY 7378 [(8-[-[4-(2-,ethoxyphenyl)-1-piperazinyl]ethyl]-8-azaspirol[4]- decane-7,9-dione-2-HCL] and spiperone, did not reduce MIA. Indeed, BMY 7378 blocked the ability of 8-OH-DPAT to antagonize MIA. Under the present conditions, agonists and antagonists at adrenergic and dopaminergic receptors did not attenuate MIA. These data show that, over a certain range of doses, the systemic administration of 8-OH-DPAT and other high efficacy 5-HT1A agonists functionally antagonizes the antinociceptive action of systemically applied morphine in a competitive-like manner. It is suggested that 5-HT1A receptors play an important role in the modulation of opioidergic antinociceptive mechanisms.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

The adverse effects of hallucinogens from intramural perspective.

UNLABELLED: Very recently, after a long-lasting, worldwide moratorium on research of hallucinogenic agents, a good number of advanced countries have been revising their position, and start to approve testing the physiological and therapeutic effects of hallucinogens in human subjects. The purpose of this article is to review safety information available in the literature on hallucinogen use, and sort out those data from the reported complications of their abuse. Because of prohibitory regulations of the last 35 years, there are difficulties in achieving this kind of evaluation. Our approach has to be broad, and at times retrospective, in contrast to the well-controlled, focused, prospective design of the premarketing trials of legal drugs. The article summarizes the analyses in anticipation of supportive regulatory changes for the use of hallucinogens in well controlled studies and strictly supervised clinical trials. KEYWORDS: adverse effects, ayahuasca, N,N-dimethyltryptamine, hallucinogenic agents, ibogaine, lysergic acid diethylamide, N-methyl-3,4-methylenedioxyamphetamine, psilocybin, therapeutic use.

Drug Interactions↗

5-hydroxytryptamine (5-HT)1A receptors and the tail-flick response. I. 8-hydroxy-2-(di-n-propylamino) tetralin HBr-induced spontaneous tail-flicks in the rat as an in vivo model of 5-HT1A receptor-mediated activity.

This study pharmacologically characterizes a novel behavioral response as a potential in vivo model of serotonin (5-HT)1A receptor-mediated activity. In rats restrained in horizontal cylinders, the selective 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino) tetralin HBr (8-OH-DPAT), dose-dependently (0.04-10.0 mg/kg s.c.) elicited spontaneous tail-flicks (STFs). This action was mimicked by other ligands possessing high affinity and high efficacy at 5-HT1A sites: RU 24969 [(5-methoxy-3-(1,2,3,6-tetrahydropyridin-4-yl)-1H-indole], lisuride, (+)-lysergic acid diethylamide and 5-methoxy-N,N-dimethyltryptamine hydrogen oxalate. The response could not be elicited by CGS 12066B [7-trifluormethyl-4-(4-methyl-l-piperazonyl)-pyrrolol- [1-2-a] quinoxaline dimaleate], mCPP 1-(3-chlorophenyl)-piperazine-2-HCl, TFMPPm-trifluromethylphenylpiperazine HCl, MK 212 [6-chloro-2-(l-piperzinyl)pyrazine], quipazine and DOI (+-)-2,5-dimethoxy-4-iodophenyl-2-aminopropane HCl, which act in vivo as agonists at 5-HT1B, 5-HT1C and/or 5-HT2 receptors, or by the 5-HT3 agonist, 2-methyl-5-HT. p-chloroamphetamine, which releases endogenous 5-HT, also evoked STFs; in contrast, d-amphetamine, a preferential releaser of catecholamines, was inactive, as were agonists and antagonists at alpha-1, alpha-2, beta-1, beta-2, dopamine D1 and D2 sites. 8-OH-DPAT-elicited STFs were blocked by the 5-HT1/2 antagonist, methiothepin, but not by the 5-HT1C/5-HT2 antagonists, mianserin, ritanserin and ICI 169,369 [2-(2-dimethylaminoetheylthio)-3-phenylquinoline] nor by the 5-HT3 antagonists, GR 38032F [(1,2,3,9-tetrahydro-9-methyl-3-[(2-methyl-1H-imidazol-l-yl)methyl]-4H- carbazol-4-one HCl], ICS 205,930 [(3 alpha-tropanyl)-1H-indol-3-carboxylic acid ester] and MDL 72222 [(1 alpha H, 3 alpha, 5 alpha H)-tripan-3-yl-3,5- dichlorobenzoate]. beta-Blockers with 5-HT1A affinity i.e., (-)-alprenolol, (+/-)-isamoltane and, stereoselectivity, (-)-but not (+)-pindolol, blocked the action of 8-OH-DPAT. Spiperone and spiroxatrine, D2 antagonists with high 5-HT1A affinity, also inhibited 8-OH-DPAT-induced STFs. Selective beta-blockers and D2 antagonists with low 5-HT1A affinity were inactive. 5-HT1A partial agonists, the pyrimidinylpiperazines, buspirone, gepirone and ipsapirone, the halogenated phenylpiperazine, LY 165,163 [1-(2-(4-aminophenyl) ethyl-4-(3-trifluoromethylphenyl)-piperazine], and the benzodioxane, MDL 72832 [8-(4-(1,4-benzodioxan-2-yl-methylamino)-butyl-8-azaspiro-(4 ,5)-decane- 7,9-dione] did not elicit STFs and antagonized the effect of 8-OH-DPAT.(ABSTRACT TRUNCATED AT 400 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗

Substance use among senior medical students. A survey of 23 medical schools.

Senior students at 23 regionally distributed medical schools received an anonymous questionnaire designed to examine current and prior use of tobacco, alcohol, and nine other drugs. The overall response rate was 67% (N = 2046). Substance use prevalence rates during the 30 days preceding the survey included alcohol, 87.5%; marijuana, 10.0%; cigarettes, 10.0%; cocaine, 2.8%; tranquilizers, 2.3%; opiates other than heroin, 1.1%; psychedelics other than LSD (lysergic acid diethylamide), 0.6%; amphetamines, 0.3%; barbiturates, 0.2%; LSD, 0.1%; and heroin, 0.0%. Compared with national, age-related comparison groups, senior medical students reported less use of all substances during the past 30 days and the past 12 months, except for alcohol, tranquilizers, and psychedelics other than LSD. Substantial new drug use after entry into medical school was reported only for tranquilizers. Seven students (0.2%) admitted to current dependence on a substance other than tobacco, four of these implicating marijuana. Thirty-three students (1.6%) believed that they currently needed help for substance abuse. Only 25.7% were aware of any policy on substance abuse at their own school.

Adult↗

Serotonin-2 receptors coupled to phosphoinositide hydrolysis in a clonal cell line.

A permanent line of cells has been established from the transplantable rat pituitary tumor 7315a. P11 cells have been cloned repeatedly, and after more than 60 passages their growth and characteristics are stable. Results of radioligand binding studies with 125I-lysergic acid diethylamide (125I-LSD) indicate that P11 cells express serotonin-2 (5-HT2) receptors. Analysis of the binding of 125I-LSD to membranes prepared from P11 cells revealed the presence of a single class of high affinity sites (Kd = 1.6 nM; Bmax = 211 fmol/mg of protein). The pharmacological profile of the inhibition of the binding of 125I-LSD by a panel of drugs was consistent with the expected profile of these drugs at 5-HT2 receptors. The affinity of the site for serotonin was in the low micromolar range and was decreased by GTP. Phosphoinositide hydrolysis in P11 cells, measured in the presence of lithium, was stimulated by serotonin. Increasing concentrations of the 5-HT2-selective antagonist ketanserin blocked phosphoinositide hydrolysis stimulated by serotonin, and Schild analysis was consistent with a simple competitive interaction. The Ki for ketanserin derived from Schild analysis was comparable to the Ki for ketanserin at the binding site for 125I-LSD. These results suggest that stimulation of phosphoinositide hydrolysis in P11 cells by serotonin is mediated by 5-HT2 receptors. Pretreatment of P11 cells with pertussis toxin caused ADP-ribosylation of Gi and Go, but did not affect the ability of serotonin to stimulate phosphoinositide hydrolysis. Therefore, the guaninine nucleotide-binding protein involved in the coupling of 5-HT2 receptors to phospholipase C in P11 cells is unlikely to be either Gi or Go. P11 cells expressing 5-HT2 receptors coupled to phosphoinositide hydrolysis will be a useful model system for future studies of the regulation and function of 5-HT2 receptors on cultured cells.

Animals↗

Serotonin receptor-mediated activation of adenylate cyclase in the neuroblastoma NCB.20: a novel 5-hydroxytryptamine receptor.

Serotonin (5-hydroxytryptamine; 5-HT) and its analogs activate adenylate cyclase in membrane particles from neuroblastoma NCB.20 cells. Low concentrations of GTP (EC50 = 60 nM) were required for activation by serotonin. Guanosine 5'-O-(2-thiodiphosphate) inhibited serotonin-activated cyclase in these cells. The nonhydrolyzable GTP analogs guanosine 5'-O-(3-thiotriphosphate) (EC50 = 3 nM) and guanylyl-imidodiphosphate (EC50 = 100 nM) substituted for GTP in potentiating serotonin activation. Pretreatment of the cells with cholera toxin potentiated enzyme activation by serotonin, whereas pertussis toxin was found to have little effect, indicating the involvement of the alpha subunit of a stimulatory GTP-binding protein in enzyme activation. Homologous desensitization of the serotonin-stimulated adenylate cyclase was demonstrated in membranes prepared from intact cells pretreated with serotonin. Cell membrane particles that were desensitized to serotonin were still responsive to beta-adrenergic agonists and to prostaglandin E1. Evidence is presented indicating that serotonin stimulation of adenylate cyclase is mediated by receptors that are distinct from other positively coupled receptors (beta-adrenergic, histamine, and prostacyclin). Equilibrium binding analysis with [3H]serotonin, [3H]lysergic acid diethylamide, and [3H]dihydroergotamine suggested that the site density was below the level of detection of binding of these radioligands. The pharmacological characteristics of the serotonin-activated cyclases were analyzed in order to compare these serotonin receptors with the family of different receptor subtypes. Correlation analysis between the potencies of different agonists and antagonists at the cyclase in these cells and their reported relative potencies for different serotonin receptor subtypes showed no correlation with the 5-HT1A, 5HT1B, 5HT1D, 5-HT2, and 5-HT3 receptors. On the other hand, the analysis showed that the NCB.20 serotonin receptors are similar but not identical to the rat and pig brain 5-HT1C receptors and to the serotonin receptors coupled to adenylate cyclase in the trematodes Schistosoma mansoni and Fasciola hepatica. The results point to a novel serotonin receptor which has a low density in these cells.

Adenosine Diphosphate Ribose↗

1-(1-Naphthyl)piperazine, a central serotonin agonist.

1-(1-Naphthyl)piperazine (1-NP) had high affinity for tritiated serotonin, tritiated LSD (lysergic acid diethylamide) and tritiated spiperone binding sites in rat brain cortex in vitro. 1-NP at doses of 3-30 mg/kg i.p. decreased 5-hydroxyindoleacetic acid (5-HIAA) concentration in whole brain of rats in vivo. The 30 mg/kg dose caused a significant increase in serum corticosterone concentration. At doses of 3-30 mg/kg i.p., 1-NP reduced the accumulation of 5-hydroxytryptophan following decarboxylase inhibition by NSD 1015 in rat hypothalamus and striatum. Reduced serotonin turnover and elevated serum corticosterone concentrations are interpreted as evidence of central serotonin receptor activation by compounds of this structural class. 1-NP has previously been reported to antagonize vascular serotonin receptors, suggesting that it, like 1-(m-trifluoromethylphenyl)piperazine, behaves as an antagonist at peripheral (vascular) serotonin receptors despite being an agonist at central serotonin receptors.

Animals↗

Antiserotonin activity of 9-methyl-2-[3-(4-phenyl-1-piperazinylpropyl)]-1,2,3,4-tetrahydro -beta-carbolin-1-one (B-193).

The effect of B-193 on the central and peripheral serotonin system was studied. B-193 antagonized the head-twitches responses induced by L-5-hydroxytryptophan (L-5-HTP) in mice (ED50 = 0.75 mg/kg ip and 6.6 mg/kg po) and lysergic acid diethylamide (LSD) in rats (ED50 = 1.54 mg/kg ip) and also counteracted forepaws clonic convulsions induced by tryptamine (ED50 = 3.07 mg/kg ip). B-193 (2.5-20 mg/kg ip) antagonized dose-dependently hyperthermia induced by fenfluramine or m-chlorophenylpiperazine (m-CPP) and in a dose of 1 mg/kg iv abolished the stimulation of the flexor reflex evoked by quipazine or fenfluramine. B-193 given in a concentration of 10(-7)-10(-5) mol/l competitively inhibited contractions of the rat stomach fundus strip induced by serotonin (5-HT) (pA2 = 6.5) and the increases in blood pressure induced by 5-HT in pithed rats (ED50 = 0.17 mg/kg iv). In receptor binding studies B-193 has shown distinct affinity to 5-HT2 receptors, and alpha 1-adrenoceptors much weaker affinity to 5-HT1 receptors and alpha 2-adrenoceptors but not to beta-adrenergic, GABA-ergic or benzodiazepine receptors. Our findings demonstrated that B-193 shows potent central and peripheral antiserotonin activity.

Animals↗

Pharmacology of 5-hydroxytryptamine-1A receptors which inhibit cAMP production in hippocampal and cortical neurons in primary culture.

Serotonin (5-hydroxytryptamine, 5-HT) inhibited the formation of cAMP promoted by vasoactive intestinal polypeptide, plus forskolin, in mouse hippocampal and cortical neurons in primary culture. The rank order of potencies of classical 5-HT1 agonists in inhibiting cAMP formation in hippocampal neurons was 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) greater than 5-carboxamidotryptamine (5-CT) greater than d-lysergic acid diethylamide greater than 5-HT greater than 5-methoxy-N,N-dimethyltryptamine (5-MeO-N,N-DMT) greater than RU 24969 greater than ipsapirone greater than bufotenine greater than buspirone [half-maximal efficacy (EC50) = 7, 18, 30, 52, 90, 102, 100, 110, and 128 nM, respectively]. All the tryptamine derivatives substituted in position 5 of the indol were potent agonists [5-HT, 5-CT, 5-MeO-N,N-DMT, 5-methoxytryptamine, and bufotenine], whereas tryptamine, N-methyltryptamine, and N,N-dimethyltryptamine were poor agonists. The most potent antagonists tested were spiperone, (+/-)-pindolol, (+/-)-cyanopindolol, WB4101, and methiothepin, the affinity of spiperone for this receptor being 22 nM. In contrast, ketanserin, a specific 5-HT2 antagonist, and 5-HT3-selective drugs (ICS 205 930 and MDL 72222) were very weak in antagonizing the 5-HT-inhibited cAMP formation. The pharmacological profiles of 5-HT receptors mediating the inhibition of cAMP formation indicate that these receptors correspond to the 5-HT1A-binding site subtypes. Experiments with the Bordetella pertussis toxin indicate that the 5-HT1A receptor mediating inhibition of cAMP production involves a pertussis toxin-sensitive GTP-binding protein. In the absence of VIP, cAMP formation could be stimulated through a 5-HT receptor, but the specific 5-HT1A agonists, 8-OH-DPAT and RU 24969 did not stimulate cAMP production. These results suggest that in mouse embryonic hippocampal neurons, the 5-HT1A receptors, which are negatively coupled to adenylate cyclase, are distinct from the receptor positively coupled to this enzyme. The pharmacological characterization of the 5-HT receptor negatively coupled to adenylate cyclase in mouse embryonic cortical neurons indicates that it differs from the 5-HT1A receptor found in hippocampal neurons. Its main differences with the 5-HT1A receptor in hippocampal neurons are as follows: 1) 8-OH-DPAT was only a poor partial agonist in cortical neurons, whereas it was the best full agonist in hippocampal neurons; and 2) metergoline and methysergide as well as the anxiolytic drugs, ipsapirone and buspirone, which were potent agonists in hippocampal neurons, were competitive antagonists in cortical neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗

[Effect of blockade of the dopamine, serotonin and cholinergic receptors on opioid modification of habituation in the visual cortex of the turtle].

Blockade of dopamine receptors by haloperidol and serotonin receptors by lysergic acid diethylamide in turtle visual cortex, effectively changes the modifying effect of agonists of opioid mu-, delta-, kappa-, and sigma-receptors: morphine, D-Ala2, D-Leu5-enkephalin, bremazocine and SKF 10.047, on dynamics of habituation of orthodromic evoked potential. Muscarinic cholinergic blocker atropine disturbs the habituation modification by morphine and bremazocine. Conclusion is made, that modifying effects of opiate agonists on habituation are the result of interaction of activated opiate and transmitter receptors.

Animals↗

Spectrophotometric and liquid chromatographic identification of 3,4-methylenedioxyphenylisopropylamine and its N-methyl and N-ethyl homologs.

3,4-Methylenedioxyphenylisopropylamine (MDA) is an hallucinogenic drug that somewhat resembles lysergic acid diethylamide (LSD) in its effects. Recently, widespread abuse of the N-methyl homolog (MDMA) of MDA has led to federal control. This article reports on the synthesis of the N-ethyl homolog (MDEA) of MDA as well as spectrophotometric and chromatographic methods for identification of the 3 homologs.

3,4-Methylenedioxyamphetamine↗

Neuroendocrine effects of setoperone: a new neuroleptic drug.

Setoperone (R 52245), a serotonin S2 and dopamine D2 receptor blocker, was tested on eight healthy male volunteers, receiving 5 or 40 mg orally, in order to assess the modifications of plasma prolactin levels, as an index of receptor blocking activity. Both doses significantly increased plasma levels, confirming the dopamine blocking activity. In vitro and in vivo studies have shown serotonin S2 receptor blockade and lysergic acid diethylamide antagonist activity. Setoperone is proposed as a possible new neuroleptic drug.

Adolescent↗

Pharmacological properties of mechanical responses of the rat oesophageal muscularis mucosae to vagal and field stimulation.

Electrical stimulation applied to vagal oesophageal branches of the isolated curarized oesophagus, or via field electrodes to the isolated tunica muscularis mucosae (TMM), increased longitudinal tension and intraluminal pressure in a frequency-dependent manner. Differences between cervical and distal TMM segments were noted in frequency-response relationships, as well as in the pulse-width dependence of contractions to field stimulation. Vagally- and field-stimulated contractions were eliminated by tetrodotoxin or hyoscine, indicating their mediation by cholinergic neurones. The field-stimulated postganglionic responses were resistant to hexamethonium or (+)-tubocurarine and weakly inhibited by morphine. Vagally- and field-stimulated TMM contractions were mimicked by muscarinic agonists, augmented by acetylcholinesterase inhibitors, and inhibited more effectively by beta-than by alpha 1-or alpha 2-adrenoceptor agonists. 5-Hydroxytryptamine (5-HT) exerted excitatory and/or inhibitory effects: TMM in situ responded with a hexamethonium-resistant, ketanserin-sensitive transient increase in tension comparable to that produced by field stimulation. In the isolated TMM, moderate excitatory responses were limited to the distal portion with inhibition predominating in the remaining proximal portion. 5-HT-induced inhibitory effects on field-stimulated tension responses were paralleled by relaxant effects on muscarinic agonist-induced tonic contractile responses, both of which were resistant to 5-HT-receptor antagonists including ketanserin, lysergic acid diethylamide (LSD), methysergide or methergoline. Field stimulation at a low frequency and pulse durations greater than 1.0 ms produced a relaxation response in preparations exposed to tetrodotoxin or hyoscine, provided that active muscle tonus was present. The relaxation in response to field stimulation was insensitive to antagonists of 5-HT, catecholamines, histamine, or indomethacin, suggesting a non-neurogenic origin. Histochemical examination of the isolated TMM preparation for cholinesterases revealed the presence of an extensive submucosal ganglionic plexus. It is concluded that: (i) intrinsic cholinergic neurones of the submucosal plexus form the final common pathway for extrinsic vagal and local (myenteric) projections to the TMM; (ii) the neural basis, if any, of non-cholinergic non-adrenergic inhibitory mechanisms remains to be established; (iii) the TMM may assist in generating propulsive oesophageal motility.

Animals↗

The effect of early postnatal hypoxia on the effectiveness of drugs influencing motor behaviour in adult rats.

The effectiveness of drugs affecting aminergic triggered motor behaviour was investigated in adult rats oxygen deprived in the early postnatal life. Offsprings were exposed to hypobaric hypoxia (pO2 = 11.6 kPa) from the 2nd till the 10th postnatal day (10 h per day). Hypoxia exposed animals displayed a significant decrease of the locomotor apomorphine effect as well as of the amphetamine induced stereotyped behaviour. On the other hand, apomorphine stereotypies and the locomotor amphetamine effect proved to be unchanged after postnatal oxygen deprivation. The motility levels achieved after giving lysergic acid diethylamide 30 min before apomorphine administration were found to be considerably higher than after apomorphine alone and similar for both controls and hypoxia exposed animals. After unilateral dopamine injections into the nucleus accumbens no different rotational behaviour was detectable. The deviations in some of their responses to drugs affecting aminergically triggered behaviour in adult rats suggested a decreased behavioural effectiveness of dopamine agonists due to early postnatal hypoxia.

Amphetamine↗

Drug use among university students in the state of São Paulo, Brazil.

A survey of drug use carried out from April 1984 to May 1985 at the University of São Paulo, Brazil, showed that of 2,475 undergraduate students surveyed, 588 respondents, or 23.8 per cent, abused drugs at some time in their lives. Drug use was somewhat more common among males (25.3 per cent) than among females (21.5 per cent). Among the drug users, the use of cannabis ranked first (41.2 per cent), followed by amphetamines (27.4 per cent), cocaine (12.2 per cent), tranquillizers (12.2 per cent), barbiturates (5.6 per cent), morphine and heroin (0.8 per cent) and lysergic acid diethylamide (0.5 per cent). Of the total number of respondents, 10 per cent were current habitual drug users, while 13.8 per cent had at some time been drug users but were no longer using drugs at the time of the survey. Of 23 postgraduate students surveyed, 10 respondents, or 43.5 per cent, used either cannabis, amphetamines or tranquillizers.

Adult↗

Problems of drug abuse and preventive measures in Poland.

An increasing abuse of drugs emerged among young people in Poland at the end of the 1960s and the beginning of the 1970s. According to information provided by the Ministry of Health and Social Welfare, there are currently 35,000 drug abusers, but the actual number is estimated at approximately 200,000. The abuse of extract from poppy straw and the inhalation of volatile solvents, such as glue and paint remover, are the major drug abuse problems. Addicts prepare a decoction of poppy straw for injection, and morphine and heroin have been clandestinely manufactured in very elementary home-made laboratories. Recently, methamphetamine hydrochloride and lysergic acid diethylamide (LSD) have also been illicitly produced in such home-made laboratories. The increasing drug abuse problem has prompted the authorities to prepare new complementary drug control legislation, the Act on the Prevention of Narcotic Addiction, which was adopted on 31 January 1985. The Act provides for more effective preventive and treatment measures, as well as severe punishment for involvement in illicit drug trafficking. Treatment, rehabilitation and social reintegration of drug-dependent persons is provided on a voluntary basis, except for persons convicted of drug-related offences and for persons under 18 years of age, in which case treatment may be compulsory.

Adolescent↗

Evidence for a presynaptic inhibitory action of 5-hydroxytryptamine in a mammalian sympathetic ganglion.

Effects of 5-hydroxytryptamine (5-HT) on synaptic transmission of isolated rabbit superior cervical ganglia were investigated by means of intracellular recording techniques. Superfusion of 5-HT (1-100 microM) onto the ganglion cells reversibly depressed the amplitude of the fast excitatory postsynaptic potential (epsp) without causing a noticeable change in the membrane potential or input resistance in the majority of cells studied. In a portion of neurons, 5-HT produced a small to moderate, transient depolarization accompanied by a fall in membrane resistance, as well as a diminution of the epsp. In these neurons, the synaptic potentials did not recover to their full amplitude even when the membrane potentials and membrane resistance had returned to the control level. The inhibitory effect of 5-HT was not antagonized by lysergic acid diethylamide (0.3-1 microM), methysergide (1-10 microM), picrotoxin (10-50 microM) and phenoxybenzamine (5 microM); the first two agents when applied alone reversibly diminished the epsp. The mean quantal content but not the quantal size of the evoked epsp was significantly reduced by 5-HT in a low Ca/high Mg solution. Lastly, 5-HT reduced the amplitude of epsp while not appreciably affecting the acetylcholine potential induced by iontophoresis of the acetylcholine onto the same ganglion cells. These results provide electrophysiological evidence suggesting that 5-HT-induced inhibition of synaptic transmission in sympathetic ganglia is primarily due to a presynaptic mechanism resulting in a reduction of the evoked release of acetylcholine.

Acetylcholine↗