Modeling motivational deficits in mouse models of schizophrenia: Behavior analysis as a guide for neuroscience

被引:32
作者
Ward, Ryan D. [1 ,3 ]
Simpson, Eleanor H. [1 ]
Kandel, Eric R. [2 ,3 ,4 ]
Balsam, Peter D. [1 ,3 ]
机构
[1] Columbia Univ, New York State Psychiat Inst, Dept Psychiat, New York, NY 10032 USA
[2] Howard Hughes Med Inst, Chevy Chase, MD 20815 USA
[3] Columbia Univ, Dept Psychiat, Cognit Neurosci Div, New York, NY 10032 USA
[4] Columbia Univ Coll Phys & Surg, Kavli Inst Brain Sci, New York, NY 10032 USA
关键词
Motivation; Schizophrenia; Animal models; Dopamine D2 receptors; Transgenic mice; NUCLEUS-ACCUMBENS DOPAMINE; D-2; RECEPTORS; SELECTIVE OVEREXPRESSION; TIME-ESTIMATION; TRANSIENT; DURATION; SYSTEM; BRAIN; MICE; IDENTIFICATION;
D O I
10.1016/j.beproc.2011.02.004
中图分类号
B84 [心理学];
学科分类号
04 ; 0402 ;
摘要
In recent years it has become possible to develop animal models of psychiatric disease in genetically modified mice. While great strides have been made in the development of genetic and neurobiological tools with which to model psychiatric disease, elucidation of neural and molecular mechanisms thought to underlie behavioral phenotypes has been hindered by an inadequate analysis of behavior. This is unfortunate given the fact that the experimental analysis of behavior has created powerful methods for isolating and describing the functional properties of behavioral mechanisms that are capable of providing deep understanding of behavioral phenotypes. A better understanding of the biological basis of normal behavior and its disturbance in psychiatric disease will require the application of these rigorous behavior analytic tools to animal models. In this review we provide an example of a merging of genetic and behavioral methods and illustrate its utility in the analysis of a mouse model of the motivational deficits in schizophrenia. The synergy between basic behavior analysis, neuroscience, and animal models of psychiatric disease has great potential for achieving a deeper understanding of behavior and its neurobiological mechanisms as well as for leading to improvements in diagnosis and treatment in clinical settings. (C) 2011 Elsevier B.V. All rights reserved.
引用
收藏
页码:149 / 156
页数:8
相关论文
共 72 条
[51]   Different behavioral effects of haloperidol, clozapine and thioridazine in a concurrent lever pressing and feeding procedure [J].
Salamone, JD ;
Cousins, MS ;
Maio, C ;
Champion, M ;
Turski, T ;
Kovach, J .
PSYCHOPHARMACOLOGY, 1996, 125 (02) :105-112
[52]   Behavioral functions of nucleus accumbens dopamine: Empirical and conceptual problems with the anhedonia hypothesis [J].
Salamone, JD ;
Cousins, MS ;
Snyder, BJ .
NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS, 1997, 21 (03) :341-359
[53]   Dopamine, behavioral economics, and effort [J].
Salamone, John D. ;
Correa, Merce ;
Farrar, Andrew M. ;
Nunes, Eric J. ;
Pardo, Marta .
FRONTIERS IN BEHAVIORAL NEUROSCIENCE, 2009, 3
[54]   Inducible gene targeting in mice using the Cre/lox system [J].
Sauer, B .
METHODS, 1998, 14 (04) :381-392
[55]   ANTIPSYCHOTIC DRUG DOSES AND NEUROLEPTIC-DOPAMINE RECEPTORS [J].
SEEMAN, P ;
LEE, T ;
CHAUWONG, M ;
WONG, K .
NATURE, 1976, 261 (5562) :717-719
[56]   Impaired hippocampal-prefrontal synchrony in a genetic mouse model of schizophrenia [J].
Sigurdsson, Torfi ;
Stark, Kimberly L. ;
Karayiorgou, Maria ;
Gogos, Joseph A. ;
Gordon, Joshua A. .
NATURE, 2010, 464 (7289) :763-U139
[57]  
SIMPSON EH, BIOL PSYCHI IN PRESS
[58]  
Skinner B.F., 1974, BEHAVIORISM
[59]  
Skinner B. F., 1965, Science and human behavior
[60]  
SKINNER BF, 1977, BEHAVIORISM, V5, P1