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3 results

  • LSD acutely impairs working memory, executive functions, and cognitive flexibility, but not risk-based decision-making

  • Thomas Pokorny, Patricia Duerler, Erich Seifritz, Franz X. Vollenweider, Katrin H. Preller
  • Journal:
    Psychological Medicine / Volume 50 / Issue 13 / October 2020
    Published online by Cambridge University Press:
    10 September 2019, pp. 2255-2264
  • Background

    Psychiatric and neurodegenerative illnesses are characterized by cognitive impairments, in particular deficits in working memory, decision-making, and executive functions including cognitive flexibility. However, the neuropharmacology of these cognitive functions is poorly understood. The serotonin (5-HT) 2A receptor might be a promising candidate for the modulation of cognitive processes. However, pharmacological studies investigating the role of this receptor system in humans are rare. Recent evidence demonstrates that the effects of Lysergic acid diethylamide (LSD) are mediated via agonistic action at the 5-HT2A receptor. Yet, the effects of LSD on specific cognitive domains using standardized neuropsychological test have not been studied.

    Methods

    We examined the acute effects of LSD (100 µg) alone and in combination with the 5-HT2A antagonist ketanserin (40 mg) on cognition, employing a double-blind, randomized, placebo-controlled, within-subject design in 25 healthy participants. Executive functions, cognitive flexibility, spatial working memory, and risk-based decision-making were examined by the Intra/Extra-Dimensional shift task (IED), Spatial Working Memory task (SWM), and Cambridge Gambling Task (CGT) of the Cambridge Neuropsychological Test Automated Battery.

    Results

    Compared to placebo, LSD significantly impaired executive functions, cognitive flexibility, and working memory on the IED and SWM, but did not influence the quality of decision-making and risk taking on the CGT. Pretreatment with the 5-HT2A antagonist ketanserin normalized all LSD-induced cognitive deficits.

    Conclusions

    The present findings highlight the role of the 5-HT2A receptor system in executive functions and working memory and suggest that specific 5-HT2A antagonists may be relevant for improving cognitive dysfunctions in psychiatric disorders.

  • 11 - Genetic factors underlying drug-induced tardive dyskinesia

  • from Part V - Specific psychotropic drugs and disorders
    • By Ronnen H. Segman, Department of Psychiatry, Hadassah-Hebrew University Medical Center, Jerusalem, Israel, Bernard Lerer, Department of Psychiatry, Hadassah-Hebrew University Medical Center, Jerusalem, Israel
  • Edited by Bernard Lerer, Hadassah-Hebrew Medical Center, Jerusalem
  • Book:
    Pharmacogenetics of Psychotropic Drugs
    Published online:
    20 August 2009
    Print publication:
    29 August 2002, pp 245-266

  • Summary

    Tardive dyskinesia (TD) affects about one fifth of schizophrenia patients following chronic exposure to dopamine receptor antagonist drugs. Drug- and patient-related risk factors for the development of TD have received much research attention but appear to predict only a minor part of the variance in the incidence of TD. This chapter reviews this rapidly developing field, incorporating recently available molecular genetic tools for a renewed exploration of the biological basis of TD. Genes coding for known drug targets can be directly explored for involvement in TD susceptibility. Genetic variability in dopamine receptors may predict functional differences in response patterns to neuroleptic agents and may be relevant to the expression of idiosyncratic reactions. Other promising findings, including the reported associations with 5-HT2A receptor (5-HTR2A) and 5-HTR2C and manganese superoxide dismutase (MnSOD) genetic polymorphic sites, require independent replications.

  • Recent developments in the genetics of schizophrenia

  • Kieran C Murphy, Michael Gill
  • Journal:
    Irish Journal of Psychological Medicine / Volume 13 / Issue 4 / December 1996
    Published online by Cambridge University Press:
    13 June 2014, pp. 151-154
    Print publication:
    December 1996

  • Objectives: To examine the evidence concerning the recent developments in the genetics of schizophrenia.

    Methods: An extensive literature search was performed and relevant papers were examined and analysed.

    Findings: There is overwhelming evidence that schizophrenia shows familial aggregation. Recent molecular genetic studies support the presence of susceptibility genes on chromosomes 6 and 22. In addition, an association between schizophrenia, the dopamine D3 receptor gene and the 5-HT2a receptor gene has also been demonstrated.

    Conclusions: Recent advances in DNA technology have paved the way for the detection of genes of major and minor effects in the aetiology of schizophrenia. If the presence of the recently identified susceptibility genes is confirmed, it is likely that these genes will be recognised in the near future.