Bobal M G, Savage L M
Department of Psychology, Behavioral Neuroscience Program, Binghamton University, State University of New York, United States.
Department of Psychology, Behavioral Neuroscience Program, Binghamton University, State University of New York, United States.
Neuroscience. 2015 Jan 29;285:260-8. doi: 10.1016/j.neuroscience.2014.11.015. Epub 2014 Nov 13.
The thalamus is a critical node for several pathways involved in learning and memory. Damage to the thalamus by trauma, disease or malnourishment can impact the effectiveness of the prefrontal cortex (PFC) and hippocampus (HPC) and lead to a profound amnesia state. Using the pyrithiamine-induced thiamine deficiency (PTD) rat model of human Wernicke-Korsakoff syndrome, we tested the hypothesis that co-infusion of the acetylcholinesterase inhibitor physostigmine across the PFC and HPC would recover spatial alternation performance in PTD rats. When cholinergic tone was increased by dual injections across the PFC-HPC, spontaneous alternation performance in PTD rats was recovered. In addition, we tested a second hypothesis that two ventral midline thalamic nuclei, the rhomboid nucleus and nucleus reuniens (Rh-Re), form a critical node needed for the recovery of function observed when cholinergic tone was increased across the PFC and HPC. By using the GABAA agonist muscimol to temporarily deactivate the Rh-Re the recovery of alternation behavior obtained in the PTD model by cholinergic stimulation across the PFC-HPC was blocked. In control pair-fed (PF) rats, inactivation of the Rh-Re impaired spontaneous alternation. However, when inactivation of the Rh-Re co-occurred with physostigmine infusions across the PFC-HPC, PF rats had normal performance. These results further demonstrate that the Rh-Re is critical in facilitating interactions between the HPC and PFC, but other redundant pathways also exist.
丘脑是参与学习和记忆的多条通路的关键节点。创伤、疾病或营养不良对丘脑造成的损伤会影响前额叶皮质（PFC）和海马体（HPC）的功能，并导致严重的失忆状态。我们使用硫胺素缺乏诱导的人类韦尼克-科尔萨科夫综合征大鼠模型，检验了以下假设：在PFC和HPC共同注入乙酰胆碱酯酶抑制剂毒扁豆碱可恢复PTD大鼠的空间交替行为表现。当通过在PFC-HPC进行双重注射来增加胆碱能张力时，PTD大鼠的自发交替行为表现得到了恢复。此外，我们还检验了第二个假设：两个腹侧中线丘脑核团，即菱形核和 reunien 核（Rh-Re），形成了一个关键节点，当PFC和HPC的胆碱能张力增加时，该节点是观察到的功能恢复所必需的。通过使用GABAA激动剂蝇蕈醇暂时使Rh-Re失活，PTD模型中通过PFC-HPC胆碱能刺激获得的交替行为恢复被阻断。在对照的配对喂养（PF）大鼠中，Rh-Re失活会损害自发交替行为。然而，当Rh-Re失活与在PFC-HPC注入毒扁豆碱同时发生时，PF大鼠表现正常。这些结果进一步证明，Rh-Re对于促进HPC和PFC之间的相互作用至关重要，但也存在其他冗余通路。
