Development of animal models for schizophrenia based on clinical evidence: Expectation for psychiatrists

Yukihiro Noda, Akihiro Mouri, Yukari Waki, Toshitaka Nabeshima

Research output: Contribution to journalReview article

7 Citations (Scopus)

Abstract

Schizophrenic patients show positive symptoms, negative symptoms and cognitive dysfunction. In humans, phencyclidine (PCP), a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, reproduces the schizophrenia-like psychosis including positive symptoms, negative symptoms and cognitive dysfunction. Ketamine, another non-competitive NMDA receptor antagonist, also reproduces a schizophrenia-like psychosis in healthy volunteers, and exaggerates the psychosis in schizophrenic patients. It has been hypothesized that insufficient glutamate neurotransmission is involved in the pathophysiology of schizophrenia. Therefore, attempts have been made to develop animal models of schizophrenia by using NMDA receptor antagonists such as PCP, ketamine and dizocilpine. In addition to pharmacological approaches, genetic approaches have been adopted to develop animal models of schizophrenia. The disrupted in schizophrenia 1 (DISC1) gene has been identified as a schizophrenia susceptibility gene based on linkage and single nucleotide polymorphism (SNP) association studies and clinical data, demonstrating that risk SNPs impact on the hippocampal structure and function in clinical and functional roles of DISC1 are analyzed in many kinds of transgenic mice developed. In this review, we focused on PCP and DISC1 transgenic animal models of schizophrenia and summarized recent evidence from several investigators. The basic researchers would need to collaborate with clinical psychiatrists to develop appropriate animal models for schizophrenia based on clinical evidence.

Original languageEnglish
Pages (from-to)47-53
Number of pages7
JournalJapanese Journal of Neuropsychopharmacology
Volume29
Issue number2
Publication statusPublished - 01-04-2009
Externally publishedYes

Fingerprint

Psychiatry
Schizophrenia
Animal Models
N-Methyl-D-Aspartate Receptors
Psychotic Disorders
Ketamine
Single Nucleotide Polymorphism
Research Personnel
Phencyclidine
Genetically Modified Animals
Dizocilpine Maleate
Synaptic Transmission
Transgenic Mice
Genes
Glutamic Acid
Healthy Volunteers
Pharmacology

All Science Journal Classification (ASJC) codes

  • Pharmacology (medical)
  • Psychiatry and Mental health
  • Pharmacology
  • Clinical Psychology

Cite this

@article{d4f639caea68432bad332a7cc31e6e2c,
title = "Development of animal models for schizophrenia based on clinical evidence: Expectation for psychiatrists",
abstract = "Schizophrenic patients show positive symptoms, negative symptoms and cognitive dysfunction. In humans, phencyclidine (PCP), a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, reproduces the schizophrenia-like psychosis including positive symptoms, negative symptoms and cognitive dysfunction. Ketamine, another non-competitive NMDA receptor antagonist, also reproduces a schizophrenia-like psychosis in healthy volunteers, and exaggerates the psychosis in schizophrenic patients. It has been hypothesized that insufficient glutamate neurotransmission is involved in the pathophysiology of schizophrenia. Therefore, attempts have been made to develop animal models of schizophrenia by using NMDA receptor antagonists such as PCP, ketamine and dizocilpine. In addition to pharmacological approaches, genetic approaches have been adopted to develop animal models of schizophrenia. The disrupted in schizophrenia 1 (DISC1) gene has been identified as a schizophrenia susceptibility gene based on linkage and single nucleotide polymorphism (SNP) association studies and clinical data, demonstrating that risk SNPs impact on the hippocampal structure and function in clinical and functional roles of DISC1 are analyzed in many kinds of transgenic mice developed. In this review, we focused on PCP and DISC1 transgenic animal models of schizophrenia and summarized recent evidence from several investigators. The basic researchers would need to collaborate with clinical psychiatrists to develop appropriate animal models for schizophrenia based on clinical evidence.",
author = "Yukihiro Noda and Akihiro Mouri and Yukari Waki and Toshitaka Nabeshima",
year = "2009",
month = "4",
day = "1",
language = "English",
volume = "29",
pages = "47--53",
journal = "Japanese Journal of Psychopharmacology",
issn = "1343-4144",
publisher = "Japanese Society of Neuropsychopharmacology",
number = "2",

}

Development of animal models for schizophrenia based on clinical evidence : Expectation for psychiatrists. / Noda, Yukihiro; Mouri, Akihiro; Waki, Yukari; Nabeshima, Toshitaka.

In: Japanese Journal of Neuropsychopharmacology, Vol. 29, No. 2, 01.04.2009, p. 47-53.

Research output: Contribution to journalReview article

TY - JOUR

T1 - Development of animal models for schizophrenia based on clinical evidence

T2 - Expectation for psychiatrists

AU - Noda, Yukihiro

AU - Mouri, Akihiro

AU - Waki, Yukari

AU - Nabeshima, Toshitaka

PY - 2009/4/1

Y1 - 2009/4/1

N2 - Schizophrenic patients show positive symptoms, negative symptoms and cognitive dysfunction. In humans, phencyclidine (PCP), a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, reproduces the schizophrenia-like psychosis including positive symptoms, negative symptoms and cognitive dysfunction. Ketamine, another non-competitive NMDA receptor antagonist, also reproduces a schizophrenia-like psychosis in healthy volunteers, and exaggerates the psychosis in schizophrenic patients. It has been hypothesized that insufficient glutamate neurotransmission is involved in the pathophysiology of schizophrenia. Therefore, attempts have been made to develop animal models of schizophrenia by using NMDA receptor antagonists such as PCP, ketamine and dizocilpine. In addition to pharmacological approaches, genetic approaches have been adopted to develop animal models of schizophrenia. The disrupted in schizophrenia 1 (DISC1) gene has been identified as a schizophrenia susceptibility gene based on linkage and single nucleotide polymorphism (SNP) association studies and clinical data, demonstrating that risk SNPs impact on the hippocampal structure and function in clinical and functional roles of DISC1 are analyzed in many kinds of transgenic mice developed. In this review, we focused on PCP and DISC1 transgenic animal models of schizophrenia and summarized recent evidence from several investigators. The basic researchers would need to collaborate with clinical psychiatrists to develop appropriate animal models for schizophrenia based on clinical evidence.

AB - Schizophrenic patients show positive symptoms, negative symptoms and cognitive dysfunction. In humans, phencyclidine (PCP), a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, reproduces the schizophrenia-like psychosis including positive symptoms, negative symptoms and cognitive dysfunction. Ketamine, another non-competitive NMDA receptor antagonist, also reproduces a schizophrenia-like psychosis in healthy volunteers, and exaggerates the psychosis in schizophrenic patients. It has been hypothesized that insufficient glutamate neurotransmission is involved in the pathophysiology of schizophrenia. Therefore, attempts have been made to develop animal models of schizophrenia by using NMDA receptor antagonists such as PCP, ketamine and dizocilpine. In addition to pharmacological approaches, genetic approaches have been adopted to develop animal models of schizophrenia. The disrupted in schizophrenia 1 (DISC1) gene has been identified as a schizophrenia susceptibility gene based on linkage and single nucleotide polymorphism (SNP) association studies and clinical data, demonstrating that risk SNPs impact on the hippocampal structure and function in clinical and functional roles of DISC1 are analyzed in many kinds of transgenic mice developed. In this review, we focused on PCP and DISC1 transgenic animal models of schizophrenia and summarized recent evidence from several investigators. The basic researchers would need to collaborate with clinical psychiatrists to develop appropriate animal models for schizophrenia based on clinical evidence.

UR - http://www.scopus.com/inward/record.url?scp=67651030990&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=67651030990&partnerID=8YFLogxK

M3 - Review article

C2 - 19562941

AN - SCOPUS:67651030990

VL - 29

SP - 47

EP - 53

JO - Japanese Journal of Psychopharmacology

JF - Japanese Journal of Psychopharmacology

SN - 1343-4144

IS - 2

ER -