Trial reportPsychopharmacology2012
P50 amplitude reduction: a nicotinic receptor-mediated deficit in first-degree relatives of schizophrenia patients.
Trial report in Psychopharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- A Meta-analytic Review of Auditory Event-Related Potential Components as Endophenotypes for Schizophrenia: Perspectives From First-Degree Relatives.Schizophrenia bulletin · 2016Pooled it
- Going up in smoke? A review of nAChRs-based treatment strategies for improving cognition in schizophrenia.Current pharmaceutical design · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleImpaired P50 gating is a putative index of genetically mediated nicotinic dysfunction in schizophrenia. However, assessment is confounded, in patients, by differential effects of smoking, symptoms, and treatment.
objectivesThis double-blind placebo-controlled study was designed to tease apart the relationships among P50, acute and chronic nicotine exposure, and familial risk. METHODS AND
resultsExperiment 1: To assess the putative effects of genetic vulnerability without other confounds, 14 unaffected relatives of schizophrenia patients and 15 controls, all nonsmokers, were tested with/without 7 mg transdermal nicotine. Family members had reduced P50 amplitude to an initial auditory stimulus, but normal P50 gating. Nicotine decreased P50 amplitude in controls; family members had a mixed response: eight decreased and six increased P50 amplitude with nicotine. Experiment 2: To assess chronic nicotine use and short-term withdrawal as a model of nicotinic dysfunction, 26 healthy smokers (14 abstinent for >12 h) received 21 mg transdermal nicotine. Chronic nicotine use, alone, did not alter P50 amplitude or gating. Short-term withdrawal resulted in decreased P50 amplitude, with no effect on P50 gating. Nicotine increased P50 amplitude in abstinent smokers and decreased it in nonabstinent smokers.
conclusionsFamilial vulnerability to schizophrenia reduces P50 amplitude. Nicotinic modulation of this deficit mirrors the effect of nicotine during smoking abstinence and suggests an "inverted-U" relationship between P50 amplitude and endogenous nicotinic activity. P50 amplitude may, therefore, be a sensitive marker of nicotinic dysfunction in individuals with familial risk for schizophrenia, which is mediated through mechanisms (e.g., α₄β₂ receptors) that are distinct from those (e.g., α₇ receptors) that mediate P50 gating.
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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.