Ferry Barbara, Herbeaux Karin, Cosquer Brigitte, Traissard Natalia, Galani Rodrigue, Cassel Jean-Christophe
Laboratoire de Neurosciences et Systèmes Sensoriels, Comportement et Cognition, UMR 5020 CNRS/Université Claude Bernard Lyon 1, GDR 2905 CNRS, Lyon Cedex 07, France.
Neurobiol Learn Mem. 2007 Jul;88(1):114-26. doi: 10.1016/j.nlm.2007.01.007. Epub 2007 Mar 13.
Conditioned odor aversion (COA) corresponds to the avoidance of an odorized-tasteless solution (conditioned stimulus, CS) previously paired with toxicosis. COA occurs only when the interstimulus interval (ISI) is kept short, suggesting that the memory trace of the odor is subject to rapid decay. Previous experiments have shown that the entorhinal cortex (EC) is involved in the acquisition of COA, since lesion of the EC rendered COA tolerant to long ISI. Because EC lesions induce a septo-hippocampal cholinergic sprouting, the present experiment investigated whether COA tolerance to long ISI may be linked to this sprouting reaction. In a first experiment, male Long-Evans rats subjected to bilateral excitotoxic EC lesions combined to intracerebroventricular infusions of the selective cholinergic immunotoxin 192 IgG-saporin were exposed to odor-toxicosis pairing using a long ISI (120 min). Results showed that EC-lesioned rats displayed COA with the long ISI but not the control groups. In rats with EC combined to 192 IgG-saporin lesions, histological analysis demonstrated no evidence for cholinergic septo-hippocampal sprouting. In a second experiment, animals with 192-IgG saporin lesion showed a marked COA with a short ISI (5 min). These results suggest that the COA with the long ISI found in rats with EC lesions might involve a functional activity related to the EC lesion-induced hippocampal cholinergic sprouting. As the injection of 192 IgG-saporin alone did not affect COA with a short ISI, our data also point to a possible role of hippocampal cholinergic neurons in the modulation of memory processes underlying COA.
条件性气味厌恶（COA）是指对先前与中毒配对的无味气味溶液（条件刺激，CS）的回避。只有当刺激间隔（ISI）保持较短时才会出现COA，这表明气味的记忆痕迹会迅速衰退。先前的实验表明，内嗅皮层（EC）参与了COA的习得，因为EC损伤使COA对长ISI具有耐受性。由于EC损伤会诱导隔-海马胆碱能发芽，本实验研究了对长ISI的COA耐受性是否可能与这种发芽反应有关。在第一个实验中，对雄性Long-Evans大鼠进行双侧兴奋性毒性EC损伤，并结合脑室内注射选择性胆碱能免疫毒素192 IgG-皂草素，使用长ISI（120分钟）使其暴露于气味-中毒配对中。结果表明，EC损伤的大鼠对长ISI表现出COA，但对照组没有。在EC联合192 IgG-皂草素损伤的大鼠中，组织学分析没有显示胆碱能隔-海马发芽的证据。在第二个实验中，192-IgG皂草素损伤的动物对短ISI（5分钟）表现出明显的COA。这些结果表明，在EC损伤的大鼠中发现的对长ISI的COA可能涉及与EC损伤诱导的海马胆碱能发芽相关的功能活动。由于单独注射192 IgG-皂草素并不影响对短ISI的COA，我们的数据还指出海马胆碱能神经元在调节COA潜在记忆过程中可能发挥的作用。
