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Phencyclidine animal models of schizophrenia: approaches from abnormality of glutamatergic neurotransmission and neurodevelopment.
Neurochem Int 2007 Jul-Sep; 51(2-4):173-84NI

Abstract

In humans, phencyclidine (PCP), a non-competitive N-methyl-d-aspartate (NMDA) receptor antagonist, reproduces a schizophrenia-like psychosis including positive symptoms, negative symptoms and cognitive dysfunction. Thus, the glutamatergic neuronal dysfunction hypothesis is one of the main explanatory hypotheses and PCP-treated animals have been utilized as an animal model of schizophrenia. The adult rodents treated with PCP repeatedly exhibit hyperlocomotion as an index of positive symptoms, a social behavioral deficit in a social interaction test and enhanced immobility in a forced swimming test as indices of negative symptoms. They also show a sensorimotor gating deficits and cognitive dysfunctions in several learning and memory tests. Some of these behavioral changes endure after withdrawal from repeated PCP treatment. Furthermore, repeated PCP treatment induces some neurochemical and neuroanatomical changes. On the other hand, the exposure to viral or environmental insult in the second trimester of pregnancy increases the probability of subsequently developing schizophrenia as an adult. NMDA receptor has been implicated in controlling the structure and plasticity of developing brain circuitry. Based on neurodevelopment hypothesis of schizophrenia, schizophrenia model rats treated with PCP at the perinatal stage is developed. Perinatal PCP treatment impairs neuronal development and induces long-lasting schizophrenia-like behaviors in adult period. Many findings suggest that these PCP animal models would be useful for evaluating novel therapeutic candidates and for confirming pathological mechanisms of schizophrenia.

Authors+Show Affiliations

Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya 466-8560, Japan.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

17669558

Citation

Mouri, Akihiro, et al. "Phencyclidine Animal Models of Schizophrenia: Approaches From Abnormality of Glutamatergic Neurotransmission and Neurodevelopment." Neurochemistry International, vol. 51, no. 2-4, 2007, pp. 173-84.
Mouri A, Noda Y, Enomoto T, et al. Phencyclidine animal models of schizophrenia: approaches from abnormality of glutamatergic neurotransmission and neurodevelopment. Neurochem Int. 2007;51(2-4):173-84.
Mouri, A., Noda, Y., Enomoto, T., & Nabeshima, T. (2007). Phencyclidine animal models of schizophrenia: approaches from abnormality of glutamatergic neurotransmission and neurodevelopment. Neurochemistry International, 51(2-4), pp. 173-84.
Mouri A, et al. Phencyclidine Animal Models of Schizophrenia: Approaches From Abnormality of Glutamatergic Neurotransmission and Neurodevelopment. Neurochem Int. 2007;51(2-4):173-84. PubMed PMID: 17669558.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Phencyclidine animal models of schizophrenia: approaches from abnormality of glutamatergic neurotransmission and neurodevelopment. AU - Mouri,Akihiro, AU - Noda,Yukihiro, AU - Enomoto,Takeshi, AU - Nabeshima,Toshitaka, Y1 - 2007/06/27/ PY - 2007/05/08/received PY - 2007/06/05/revised PY - 2007/06/07/accepted PY - 2007/8/3/pubmed PY - 2007/10/27/medline PY - 2007/8/3/entrez SP - 173 EP - 84 JF - Neurochemistry international JO - Neurochem. Int. VL - 51 IS - 2-4 N2 - In humans, phencyclidine (PCP), a non-competitive N-methyl-d-aspartate (NMDA) receptor antagonist, reproduces a schizophrenia-like psychosis including positive symptoms, negative symptoms and cognitive dysfunction. Thus, the glutamatergic neuronal dysfunction hypothesis is one of the main explanatory hypotheses and PCP-treated animals have been utilized as an animal model of schizophrenia. The adult rodents treated with PCP repeatedly exhibit hyperlocomotion as an index of positive symptoms, a social behavioral deficit in a social interaction test and enhanced immobility in a forced swimming test as indices of negative symptoms. They also show a sensorimotor gating deficits and cognitive dysfunctions in several learning and memory tests. Some of these behavioral changes endure after withdrawal from repeated PCP treatment. Furthermore, repeated PCP treatment induces some neurochemical and neuroanatomical changes. On the other hand, the exposure to viral or environmental insult in the second trimester of pregnancy increases the probability of subsequently developing schizophrenia as an adult. NMDA receptor has been implicated in controlling the structure and plasticity of developing brain circuitry. Based on neurodevelopment hypothesis of schizophrenia, schizophrenia model rats treated with PCP at the perinatal stage is developed. Perinatal PCP treatment impairs neuronal development and induces long-lasting schizophrenia-like behaviors in adult period. Many findings suggest that these PCP animal models would be useful for evaluating novel therapeutic candidates and for confirming pathological mechanisms of schizophrenia. SN - 0197-0186 UR - https://www.unboundmedicine.com/medline/citation/17669558/Phencyclidine_animal_models_of_schizophrenia:_approaches_from_abnormality_of_glutamatergic_neurotransmission_and_neurodevelopment_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0197-0186(07)00171-4 DB - PRIME DP - Unbound Medicine ER -