CoChat
Sign Up
Cited by 690Nicotinic Acetylcholine Receptors StudySchizophrenia research and treatmentNeuroscience and Neuropharmacology Research

The DOI matches its Crossref record; 54 of the 55 references it cites were found in a registry or an index.

Evidence in postmortem brain tissue for decreased numbers of hippocampal nicotinic receptors in schizophrenia

Freedman, Robert, Hall, Michael, Adler, Lawrence E., Leonard, Sherry·1995·Biological Psychiatry
DOI 10.1016/0006-3223(94)00252-x
Open this paper in CoChat — free account

Abstract

This study tests the hypothesis that nicotinic cholinergic receptors, including those sensitive to the antagonist alpha-bungarotoxin, are decreased in the hippocampus of schizophrenics. The hypothesis is derived from the finding that alpha-bungarotoxin causes a defect in the inhibitory gating of auditory-evoked potentials in laboratory animals that resembles a defect in auditory sensory gating observed in schizophrenics. Nicotine transiently normalizes this psychophysiological deficit in schizophrenic patients. Postmortem brain tissue was obtained from eight schizophrenic and eight age-matched nonschizophrenic subjects. Sections of the hippocampus were labeled with [125I alpha-bungarotoxin and imagined by autoradiography. Binding of the nicotinic agonist [3H]-cytisine was determined in tissue homogenates. alpha-Bungarotoxin labeled a population of putative interneurons in the hippocampus, primarily in the dentate gyrus and the CA3 region of Ammon's horn. This labeling was significantly decreased in the tissue from the schizophrenic patients, with seven or eight patients below the range of the nonschizophrenic subjects. There was also a significant decrease in the binding of cytisine. The results were not related to generalized hippocampal cell loss, drug exposure at time of death, or smoking history. This initial study suggests that schizophrenic patients have fewer nicotinic receptors in the hippocampus, a condition which may lead to failure of cholinergic activation of inhibitory interneurons, manifest clinically as decreased gating of response to sensory stimulation.

Overview

Integrity signals

Registry

Crossref · 10.1016/0006-3223(94)00252-x

Cites

54 of 54 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Research works printed but not linked: 3

  1. Daviss, 1993, Calbindin- and calretinin-immunoreactive local circuit neurons are increased in density in the prefrontal cortex of schizophrenic subjects, Neurosci Abstracts, 19, 201
  2. Goff, 1980, Neural origins of long latency evoked potentials recorded from the depth and from the cortical surface of the brain in man, Prog Clin Neurophysiol, 7, 126
  3. Klein, 1991, On the influence of smoking upon smooth pursuit eye movements of schizophrenics and normal controls, J Psychophysiology, 5, 361

Cited by

Sorted by citations

See all 690

Related

See all

Metadata

Authors
Freedman, R., Hall, M., Adler, L. E., & Leonard, S.
Affiliations
  • Denver VA Medical Center (US)
  • University of Colorado Denver (US)
Corresponding author
Freedman, Robert
ORCID
Venue
Biological Psychiatry
Publisher
Elsevier BV
Published
1995-07
Volume
38
Issue
1
Pages
22-33
ISSN
0006-3223 (ISSN-L)
DOI
10.1016/0006-3223(94)00252-x
OpenAlex
W2090019512
Cited by
678
References
55
Citations by year
2026: 2 · 2025: 10 · 2024: 8 · 2023: 12 · 2022: 11 · 2021: 16 · 2020: 18 · 2019: 17 · 2018: 11 · 2017: 17 · 2016: 18 · 2015: 34 · 2014: 29 · 2013: 27 · 2012: 30
FWCI
3.72
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Biological Psychiatry (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (1k01mh000728-01a1)
  • National Institute of Mental Health (MH-44212, MH00728, MH 38321, P50MH044212)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
  • Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
schizophrenia, nicotinic acetylcholine receptors, hippocampus, alpha-bungarotoxin binding, auditory gating, inhibitory interneurons, dentate gyrus, CA3 region, postmortem brain, cholinergic dysfunction
MeSH terms
Quinolizidine Alkaloids, Adult, Aged, Alkaloids, Autoradiography, Azocines, Binding Sites, Bungarotoxins, Cell Count, Female, Hippocampus, Humans, Image Processing, Computer-Assisted, Male, Middle Aged, Quinolizines, Receptors, Nicotinic, Schizophrenia, Cholinergic Agents, Dentate Gyrus, Culture Techniques

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review