The role of mesolimbic and nigrostriatal dopamine in latent inhibition as measured with the conditioned taste aversion paradigm
The role of mesolimbic and nigrostriatal dopamine in latent inhibition as measured with the conditioned taste aversion paradigm
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DOI：
10.1007/s002130050170
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发表时间：
1997-01-01
影响因子：
3.4
通讯作者：
Cools, AR
中科院分区：
文献类型：
--
作者：
Ellenbroek, BA;Knobbout, DA;Cools, AR
当与强化物结合时，重复呈现非强化刺激通常会延迟对该刺激的调节。这种现象称为潜在抑制。由于全身给予安非他明后潜在抑制受到干扰，本研究使用条件性味觉厌恶（CTA）范式研究了中脑边缘和黑质纹状体多巴胺末端场在潜在抑制中的作用。在此范例中，使用 5% 蔗糖溶液作为测试刺激物，使用氯化锂 (LiCl) 作为 CTA 诱导药物。在注射 LiCl 后 24 小时，通过测量两瓶蔗糖/水选择范例中的蔗糖偏好来评估 CTA 程度。由于条件性味觉厌恶迄今为止尚未用于评估多巴胺在潜在抑制中的作用，因此我们首先研究了全身应用安非他明的效果。结果表明，腹腔注射 0.25 或 0.5 mg/kg d-苯丙胺硫酸盐（在预暴露和调理时给予）通过选择性降低预暴露组中的蔗糖偏好，显着破坏了潜在抑制。这不能归因于暴露前蔗糖摄入量的减少或安非他明本身的条件性味觉厌恶作用。实验2中，在预暴露和调理阶段，将10μg/0.5μl安非他明局部双侧注射至伏隔核或背侧纹状体，之后让大鼠饮酒固定时间。结果显示，纹状体内注射安非他明后，潜在抑制显着减少，但伏隔内注射安非他明后，潜伏抑制却没有显着减少。然而，在伏隔内注射安非他明可以显着减少预暴露和调节过程中的液体摄入量。因此，在实验 3 中，我们重复了该实验，但在预暴露和调节期间仅允许动物饮用有限量的液体。结果再次表明，在纹状体内而非伏隔内注射安非他明后，潜在抑制被破坏。这些实验强调了黑质纹状体多巴胺系统在破坏潜在抑制方面的重要性，至少在使用条件性味觉厌恶范式时是如此。讨论了背侧纹状体影响潜在抑制的可能机制。
Repeatedly presenting a non-reinforced stimulus normally retards conditioning to this stimulus when it is coupled to a reinforcer. This phenomenon is called latent inhibition. Since latent inhibition is disturbed after systemic administration of amphetamine, the present study investigated the role of the mesolimbic and nigrostriatal dopamine terminal fields in latent inhibition using a conditioned taste aversion (CTA) paradigm. In this paradigm, a 5% sucrose solution was used as the test stimulus and lithium chloride (LiCl) as the CTA inducing drug. The degree of CTA was assessed by measuring the sucrose preference in a two-bottle sucrose/water choice paradigm 24 h after the LiCl injection. Since conditioned taste aversion has so far not been used to evaluate the role of dopamine in latent inhibition, we first studied the effects of systemic application of amphetamine. The results show that intraperitoneal injections of 0.25 or 0.5 mg/kg d-amphetamine sulphate (given at preexposure and conditioning) significantly disrupted latent inhibition, by selectively reducing sucrose preference in the preexposed group. This could not be attributed to a reduced sucrose intake during preexposure or to a conditioned taste aversion effect of amphetamine itself. In experiment 2 local bilateral administration of 10 mu g/0.5 mu l amphetamine into the nucleus accumbens or the dorsal striatum was given in the pre-exposed and the conditioning phase, after which the rats were allowed to drink for a fixed period of time. The results show a significant reduction in latent inhibition after intrastriatal, but not after intra-accumbens injections of amphetamine. Intraaccumbens injections of amphetamine, however, significantly reduced fluid intake during preexposure and conditioning. In experiment 3, we therefore repeated this experiment, but allowed the animals to drink only a restricted amount of liquid during preexposure and conditioning. Again the results show a disruption of latent inhibition after intrastriatal, but not intra-accumbens injections of amphetamine. These experiments emphasize the importance of the nigrostriatal dopamine system in the disruption of latent inhibition, at least when using the conditioned taste aversion paradigm. A possible mechanism by which the dorsal striatum might influence latent inhibition is discussed.