Steckler T, Sahgal A, Aggleton J P, Drinkenburg W H
Max Planck Institute of Psychiatry, Clinical Institute, Munich, Germany.
Prog Neurobiol. 1998 Feb;54(3):333-48. doi: 10.1016/s0301-0082(97)00062-2.
In the first part of three overviews on recognition memory in the rat, we discussed the tasks employed to study recognition memory. In the second part, we discussed the neuroanatomical systems thought to be of importance for the mediation of recognition memory in the rat. In particular, we delineated two parallel-distributed neuronal networks, one that is essential for the processing of non-spatial/item recognition memory processes and incorporates the cortical association areas such as TE1, TE2 and TE3, the rhinal cortices, the mediodorsal thalamic nucleus and prefrontal cortical areas (Network 1), the other comprising of the hippocampus, mamillary bodies, anterior thalamic nuclei and medial prefrontal areas (Network 2), suggested to be pivotal for the processing of spatial recognition memory. The next step will progress to the level of the neurotransmitters thought to be involved. Current data suggest that the majority of drugs have non-specific, i.e. delay-independent effects in tasks measuring recognition memory. This may be due to attentional, motivational or motoric changes. Alternatively, delay-independent effects may result from altered acquisition/encoding rather than from altered retention. Furthermore, the neurotransmitter systems affected by these drugs could be important as modulators rather than as mediators of recognition memory per se. It could, of course, also be the case that systemic treatment induces non-specific effects which overshadow any specific, delay-dependent, effect. This possibility receives support from lesion experiments (for example, of the septohippocampal cholinergic system) or studies employing local intracerebral infusion techniques. However, it is evident that those delay-dependent effects are relatively subtle and more readily seen in delayed response paradigms, which tax spatial recognition memory. One interpretation of these results could be that some neurotransmitter systems are more involved in spatial than in item recognition memory processes. However, performance in delayed response tasks can be aided by mediating strategies. Drugs or lesions can alter those strategies, which could equally explain some of the (delay-dependent) drug effects on delayed responding. Thus, it is evident that neither of the neurotransmitter systems reviewed (glutamate, GABA, acetylcholine, serotonin, dopamine and noradrenaline) can be viewed as being directly and exclusively concerned with storage/retention. Rather, our model of recognition memory suggests that information about previously encountered items is differentially processed by distinct neural networks and is not mediated by a single neurotransmitter type.
在关于大鼠识别记忆的三篇综述的第一部分中，我们讨论了用于研究识别记忆的任务。在第二部分中，我们讨论了被认为对大鼠识别记忆的介导至关重要的神经解剖系统。特别地，我们描绘了两个并行分布的神经元网络，一个对于非空间/项目识别记忆过程的处理至关重要，它包含诸如TE1、TE2和TE3等皮质联合区、鼻周皮质、丘脑背内侧核和前额叶皮质区域（网络1）；另一个由海马体、乳头体、前丘脑核和内侧前额叶区域组成（网络2），被认为对空间识别记忆的处理至关重要。下一步将深入到被认为涉及的神经递质层面。目前的数据表明，大多数药物在测量识别记忆的任务中具有非特异性，即与延迟无关的效应。这可能是由于注意力、动机或运动方面的变化。或者，与延迟无关的效应可能源于获取/编码的改变而非保持的改变。此外，受这些药物影响的神经递质系统作为识别记忆的调节剂而非介质可能很重要。当然，也有可能全身治疗会诱导出非特异性效应，从而掩盖任何特定的、与延迟相关的效应。这种可能性得到了损伤实验（例如，海马隔胆碱能系统的损伤实验）或采用局部脑内灌注技术的研究的支持。然而，很明显，那些与延迟相关的效应相对较为细微，并且在考验空间识别记忆的延迟反应范式中更容易观察到。对这些结果的一种解释可能是，一些神经递质系统在空间识别记忆过程中比在项目识别记忆过程中涉及得更多。然而，延迟反应任务中的表现可以通过介导策略得到帮助。药物或损伤可以改变这些策略，这同样可以解释一些（与延迟相关的）药物对延迟反应的影响。因此，很明显，所综述的神经递质系统（谷氨酸、γ-氨基丁酸、乙酰胆碱、血清素、多巴胺和去甲肾上腺素）都不能被视为直接且唯一地与存储/保持相关。相反，我们的识别记忆模型表明，关于先前遇到的项目的信息由不同的神经网络进行差异处理，并且不是由单一类型的神经递质介导的。
