Gestational methylazoxymethanol acetate administration: A developmental disruption model of schizophrenia

被引:183
作者
Lodge, Daniel J. [1 ]
Grace, Anthony A.
机构
[1] Univ Pittsburgh, Dept Neurosci, Pittsburgh, PA 15260 USA
关键词
MAM; Animal model; Schizophrenia; Hippocampus; Prefrontal cortex; Dopamine; Psychosis; INDUCED DOPAMINE RELEASE; WORKING-MEMORY DEFICITS; GAMMA-AMINOBUTYRIC-ACID; GABA UPTAKE SITES; PREFRONTAL CORTEX; ANIMAL-MODEL; NUCLEUS-ACCUMBENS; BIPOLAR DISORDER; RISK-FACTORS; EXTRACELLULAR DOPAMINE;
D O I
10.1016/j.bbr.2009.01.031
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
Animal models are critical for the study of psychiatric disorders since they allow the use of invasive methods that cannot be used for ethical reasons in humans. Currently there are three general models of schizophrenia; (i) those produced with acute pharmacological intervention (i.e. W-801, ketamine, PCP and amphetamine), (ii) genetic models (i.e. mutant DISC-1, D(2)-R over expression) and (iii) developmental disruption models (i.e. MAM, neonatal ventral hippocampal lesion, isolation rearing, maternal infection). Here we review evidence for the validity of gestational (day 17) MAM administration as a developmental disruption rodent model of schizophrenia. Offspring from MAM-treated dams are reported to display deficits consistent with those observed in schizophrenia patients, including anatomical changes, behavioral deficits and altered neuronal information processing. Thus gestational MAM administration has been demonstrated to induce a pathodevelopmental process leading to neuroanatomical and behavioral phenotypes consistent with that observed in schizophrenia in humans. (C) 2009 Elsevier B.V. All rights reserved.
引用
收藏
页码:306 / 312
页数:7
相关论文
共 110 条
[1]   Sub-chronic psychotomimetic phencyclidine induces deficits in reversal learning and alterations in parvalbumin-immunoreactive expression in the rat (Reprinted from vol 21, pg 198-205, 2007) [J].
Abdul-Monim, Z. ;
Neill, J. C. ;
Reynolds, G. P. .
JOURNAL OF PSYCHOPHARMACOLOGY, 2016, 30 (11) :198-205
[2]   Increased baseline occupancy of D2 receptors by dopamine in schizophrenia [J].
Abi-Dargham, A ;
Rodenhiser, J ;
Printz, D ;
Zea-Ponce, Y ;
Gil, R ;
Kegeles, LS ;
Weiss, R ;
Cooper, TB ;
Mann, JJ ;
Van Heertum, RL ;
Gorman, JM ;
Laruelle, M .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (14) :8104-8109
[3]   Do we still believe in the dopamine hypothesis? New data bring new evidence [J].
Abi-Dargham, A .
INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY, 2004, 7 :S1-S5
[4]   GENE-EXPRESSION FOR GLUTAMIC-ACID DECARBOXYLASE IS REDUCED WITHOUT LOSS OF NEURONS IN PREFRONTAL CORTEX OF SCHIZOPHRENICS [J].
AKBARIAN, S ;
KIM, JJ ;
POTKIN, SG ;
HAGMAN, JO ;
TAFAZZOLI, A ;
BUNNEY, WE ;
JONES, EG .
ARCHIVES OF GENERAL PSYCHIATRY, 1995, 52 (04) :258-266
[5]  
ANDREASEN NC, 1995, ARCH GEN PSYCHIAT, V52, P341
[6]   DIAGNOSIS AND CLASSIFICATION OF SCHIZOPHRENIA [J].
ANDREASEN, NC ;
CARPENTER, WT .
SCHIZOPHRENIA BULLETIN, 1993, 19 (02) :199-214
[7]  
BALDUINI W, 1991, NEUROTOXICOLOGY, V12, P179
[8]  
Bayer Shirley A., 1995, P1041
[9]   Ketamine-induced loss of phenotype of fast-spiking interneurons is mediated by NADPH-oxidase [J].
Behrens, M. Margarita ;
Ali, Sameh S. ;
Dao, Diep N. ;
Lucero, Jacinta ;
Shekhtman, Grigoriy ;
Quick, Kevin L. ;
Dugan, Laura L. .
SCIENCE, 2007, 318 (5856) :1645-1647
[10]   Up-regulation of GABA(A) receptor binding on neurons of the prefrontal cortex in schizophrenic subjects [J].
Benes, FM ;
Vincent, SL ;
Marie, A ;
Khan, Y .
NEUROSCIENCE, 1996, 75 (04) :1021-1031