Double dissociation of the effects of selective nucleus accumbens core and shell lesions on impulsive-choice behaviour and salience learning in rats

被引:140
作者
Pothuizen, HHJ [1 ]
Jongen-Rêlo, AL [1 ]
Feldon, J [1 ]
Yee, BK [1 ]
机构
[1] Swiss Fed Inst Technol Zurich, Lab Behav Neurobiol, CH-8603 Schwerzenbach, Switzerland
关键词
behavioural inhibition; delayed reinforcement; DRL; latent inhibition; ventral striatum;
D O I
10.1111/j.1460-9568.2005.04388.x
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The nucleus accumbens can be subdivided into at least two anatomically distinct subregions: a dorsolateral 'core' and a ventromedial 'shell', and this distinction may extend to a functional dissociation. Here, we contrasted the effects of selective excitotoxic core and medial shell lesions on impulsive-choice behaviour using a delayed reward choice paradigm and a differential reward for low rates of responding (DRL) test, against a form of salience learning known as latent inhibition (LI). Core lesions led to enhanced impulsive choices as evidenced by a more pronounced shift from choosing a continuously reinforced lever to a partially reinforced lever, when a delay between lever press and reward delivery was imposed selectively on the former. The core lesions also impaired performance on a DRL task that required withholding the response for a fixed period of time in order to earn a reward. Medial shell lesions had no effect on these two tasks, but abolished the LI effect, as revealed by the failure of stimulus pre-exposure to retard subsequent conditioning to that stimulus in an active avoidance procedure in the lesioned animals. As expected, selective core lesions spared LI. The double dissociations demonstrated here support a functional segregation between nucleus accumbens core and shell, and add weight to the hypothesis that the core, but not the shell, subregion of the nucleus accumbens is preferentially involved in the control of choice behaviour under delayed reinforcement conditions and in the inhibitory control of goal-directed behaviour.
引用
收藏
页码:2605 / 2616
页数:12
相关论文
共 57 条
  • [11] Differential involvement of the core and shell subregions of the nucleus accumbens in conditioned cue-induced reinstatement of cocaine seeking in rats
    Fuchs, RA
    Evans, KA
    Parker, MC
    See, RE
    [J]. PSYCHOPHARMACOLOGY, 2004, 176 (3-4) : 459 - 465
  • [12] Latent inhibition is disrupted by nucleus accumbens shell lesion but is abnormally persistent following entire nucleus accumbens lesion: The neural site controlling the expression and disruption of the stimulus preexposure effect
    Gal, G
    Schiller, D
    Weiner, I
    [J]. BEHAVIOURAL BRAIN RESEARCH, 2005, 162 (02) : 246 - 255
  • [13] OVERSHADOWING OF A STIMULUS-REINFORCER ASSOCIATION BY AN INSTRUMENTAL RESPONSE
    GARRUD, P
    GOODALL, G
    MACKINTOSH, NJ
    [J]. QUARTERLY JOURNAL OF EXPERIMENTAL PSYCHOLOGY SECTION B-COMPARATIVE AND PHYSIOLOGICAL PSYCHOLOGY, 1981, 33 (MAY): : 123 - 135
  • [14] Gating of information flow within the limbic system and the pathophysiology of schizophrenia
    Grace, AA
    [J]. BRAIN RESEARCH REVIEWS, 2000, 31 (2-3) : 330 - 341
  • [16] Latent inhibition: the nucleus accumbens connection revisited
    Gray, JA
    Moran, PM
    Grigoryan, G
    Peters, SL
    Young, AMJ
    Joseph, MH
    [J]. BEHAVIOURAL BRAIN RESEARCH, 1997, 88 (01) : 27 - 34
  • [17] THE NEUROPSYCHOLOGY OF SCHIZOPHRENIA
    GRAY, JA
    FELDON, J
    RAWLINS, JNP
    SMITH, AD
    HEMSLEY, DR
    [J]. BEHAVIORAL AND BRAIN SCIENCES, 1991, 14 (01) : 1 - 19
  • [18] The role of mesolimbic dopaminergic and retrohippocampal afferents to the nucleus accumbens in latent inhibition: Implications for schizophrenia
    Gray, JA
    Joseph, MH
    Hemsley, DR
    Young, AMJ
    Warburton, EC
    Boulenguez, P
    Grigoryan, GA
    Peters, SL
    Rawlins, JNP
    Taib, CT
    Yee, BK
    Cassaday, H
    Weiner, I
    Gal, G
    Gusak, O
    Joel, D
    Shadach, E
    Shalev, U
    Tarrasch, R
    Feldon, J
    [J]. BEHAVIOURAL BRAIN RESEARCH, 1995, 71 (1-2) : 19 - 31
  • [19] Gray JA, 1982, NEUROPSYCHOLOGY ANXI
  • [20] Heimer L, 1997, J NEUROPSYCH CLIN N, V9, P354