Evidence map›Paper›PMID 24595504›Full record

ArticlePsychopharmacology2014

Effects of the nicotinic α7 receptor partial agonist GTS-21 on NMDA-glutamatergic receptor related deficits in sensorimotor gating and recognition memory in rats.

Patrick M Callahan, Alvin V Terry, Ashok Tehim

Open access · greenAbstract read
In one paragraph

Article in Psychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.7field-weighted citation impact, top 10% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 37 citations in OpenAlex.

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  18. R-(+) and S-(-) isomers of cotinine augment cholinergic responses in vitro and in vivo.The Journal of pharmacology and experimental therapeutics · 2015
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 1 country.

Patrick M CallahanDepartment of Pharmacology and Toxicology, Small Animal Behavior Core, Georgia Regents University, Augusta, GA, 30912, USA, pcallahan@gru.edu.
Alvin V Terry
Ashok Tehim
Augusta University · USDr. Reddy's Laboratories (United States) · USGeorgia Regents Medical Center · US

Funding

Procognitive and Antipsychotic Actions of JWS-USC-75-IXR21AG032140 · NIA · AUGUSTA UNIVERSITY · PI TERRY, ALVIN V · 2008 to 2009
$351k
NIA NIH HHS AG032140NIA NIH HHS R21 AG032140
6 · The paper itself

Abstract

rationaleDisturbances in information processing and cognitive function are key features of schizophrenia. Nicotinic α7 acetylcholine receptors (α7-nAChR) are involved in sensory gating and cognition, thereby representing a viable therapeutic strategy. OBJECTIVES AND

methodsWe investigated the effects of GTS-21, an α7-nAChR partial agonist, on prepulse inhibition (PPI) of acoustic startle in two pharmacologic impairment models in Wistar male rats: NMDA-glutamate receptor antagonism by MK-801 and dopamine receptor agonism by apomorphine. The cognitive effects of GTS-21 were assessed using the object recognition task (ORT) at short (3 h) and long (48 h) delays in Sprague-Dawley male rats. Pharmacological specificity was assessed by methyllycaconitine (MLA) coadministration with GTS-21.

resultsIn the PPI task, GTS-21 (1-10 mg/kg) alone did not alter the PPI response or startle amplitude. Coadministration of GTS-21 with MK-801 (0.1 mg/kg) or apomorphine (0.5 mg/kg) abolished the pharmacologic-induced PPI impairment as did the antipsychotics clozapine (5.0 mg/kg) and haloperidol (0.3 mg/kg). MK-801 alone increased startle amplitude which was blocked by GTS-21. In the ORT, GTS-21 (0.1-10 mg/kg) reversed the MK-801 (0.08 mg/kg)-induced memory deficit at the 3 h delay and enhanced memory at the 48 h delay, an effect abolished by MLA (0.313-5 mg/kg).

conclusionsThe results extend our preclinical pharmacological understanding of GTS-21 to include the ability of GTS-21 to modulate NMDA-glutamate receptor function, in vivo. Given the role of NMDA-glutamate receptor involvement in schizophrenia, α7-nAChR agonists may represent a novel treatment strategy for the pathophysiological deficits of schizophrenia and other psychiatric disorders.

Indexed as

alpha7 Nicotinic Acetylcholine ReceptorAnimalsApomorphineBenzylidene CompoundsClozapineCognitionDizocilpine MaleateExcitatory Amino Acid AntagonistsGABA AntagonistsHaloperidolMaleNicotinic AgonistsPyridinesRatsRats, Sprague-DawleyRats, Wistar3-(2,4-dimethoxybenzylidene)anabaseinealpha7 Nicotinic Acetylcholine ReceptorApomorphineBenzylidene CompoundsClozapineDizocilpine MaleateExcitatory Amino Acid AntagonistsGABA AntagonistsHaloperidolNicotinic AgonistsPyridinesReceptors, NicotinicReceptors, N-Methyl-D-Aspartate

Identifiers

PMID24595504
PMCPMC4748388
OpenAlexW1992761569

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

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.