ArticlePsychopharmacology2015
PCP-based mice models of schizophrenia: differential behavioral, neurochemical and cellular effects of acute and subchronic treatments.
Article in Psychopharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Quantifying the inverted U: A meta-analysis of prefrontal dopamine, D1 receptors, and working memory.Behavioral neuroscience · 2022Pooled it
- Telmisartan mitigates behavioral and cytokine level alterations but impairs spatial working memory in a phencyclidine-induced mouse model of schizophrenia.Psychopharmacology · 2025Article
- Schizophrenia pathology reverse-translated into mouse shows hippocampal hyperactivity, psychosis behaviors and hyper-synchronous events.Molecular psychiatry · 2025Article
- Neural Mechanism of 5-HT4R-Mediated Memory Enhancement in Hippocampal-Prefrontal Circuits in a Mouse Model of Schizophrenia.International journal of molecular sciences · 2025Article
- Deficits in medial prefrontal cortex parvalbumin expression and distraction-dependent memory in rats and mice in the sub-chronic phencyclidine model for schizophrenia.Frontiers in cellular neuroscience · 2025Article
- A New Three-Hit Mouse Model of Neurodevelopmental Disorder with Cognitive Impairments and Persistent Sociability Deficits.Brain sciences · 2024Article
- Drug-induced change in transmitter identity is a shared mechanism generating cognitive deficits.Nature communications · 2024Article
- Nicotine's Effects on Schizophrenia-like Symptoms in a Mice Model: Time Matters.Brain sciences · 2024Article
- Advances in the study of phencyclidine-induced schizophrenia-like animal models and the underlying neural mechanisms.Schizophrenia (Heidelberg, Germany) · 2024Review
- Effect of intermittent subchronic MK-801 administration on dopamine synthesis capacity and responsiveness in the prefrontal cortex.Neuropsychopharmacology reports · 2024Article
- TrkB receptor interacts with mGluScience advances · 2024Article
- Drug-induced change in transmitter identity is a shared mechanism generating cognitive deficits.Research square · 2023Article
- Dual Role of the P2X7 Receptor in Dendritic Outgrowth during Physiological and Pathological Brain Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Neural substrates of cognitive impairment in a NMDAR hypofunction mouse model of schizophrenia and partial rescue by risperidone.Frontiers in cellular neuroscience · 2023Article
- NX210c Peptide Promotes Glutamatergic Receptor-Mediated Synaptic Transmission and Signaling in the Mouse Central Nervous System.International journal of molecular sciences · 2022Article
- Advantages and Limitations of Animal Schizophrenia Models.International journal of molecular sciences · 2022Review
- Modified climbing fiber/Purkinje cell synaptic connectivity in the cerebellum of the neonatal phencyclidine model of schizophrenia.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- In Vitro and In Vivo Pharmaco-Toxicological Characterization of 1-Cyclohexyl-x-methoxybenzene Derivatives in Mice: Comparison with Tramadol and PCP.International journal of molecular sciences · 2021Article
- Local circuit allowing hypothalamic control of hippocampal area CA2 activity and consequences for CA1.eLife · 2021Article
- Behavioral Tasks Evaluating Schizophrenia-like Symptoms in Animal Models: A Recent Update.Current neuropharmacology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleN-methyl-D-aspartate receptor (NMDA-R) hypofunction has been proposed to account for the pathophysiology of schizophrenia. Thus, NMDA-R blockade has been used to model schizophrenia in experimental animals. Acute and repeated treatments have been successfully tested; however, long-term exposure to NMDA-R antagonists more likely resembles the core symptoms of the illness.
objectivesTo explore whether schizophrenia-related behaviors are differentially induced by acute and subchronic phencyclidine (PCP) treatment in mice and to examine the neurobiological bases of these differences.
resultsSubchronic PCP induced a sensitization of acute locomotor effects. Spontaneous alternation in a T-maze and novel object recognition performance were impaired after subchronic but not acute PCP, suggesting a deficit in working memory. On the contrary, reversal learning and immobility in the tail suspension test were unaffected. Subchronic PCP significantly reduced basal dopamine but not serotonin output in medial prefrontal cortex (mPFC) and markedly decreased the expression of tyrosine hydroxylase in the ventral tegmental area. Finally, acute and subchronic PCP treatments evoked a different pattern of c-fos expression. At 1 h post-treatment, acute PCP increased c-fos expression in many cortical regions, striatum, thalamus, hippocampus, and dorsal raphe. However, the increased c-fos expression produced by subchronic PCP was restricted to the retrosplenial cortex, thalamus, hippocampus, and supramammillary nucleus. Four days after the last PCP injection, c-fos expression was still increased in the hippocampus of subchronic PCP-treated mice.
conclusionsAcute and subchronic PCP administration differently affects neuronal activity in brain regions relevant to schizophrenia, which could account for their different behavioral effects.
Indexed as
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.