Yamaguchi Shinji, Aoki Naoya, Kobayashi Daisuke, Kitajima Takaaki, Iikubo Eiji, Katagiri Sachiko, Matsushima Toshiya, Homma Koichi J
Faculty of Pharmaceutical Sciences, Teikyo University, Kaga, Itabashi-ku, Tokyo, Japan.
Neuroreport. 2011 Dec 7;22(17):929-34. doi: 10.1097/WNR.0b013e32834d0be7.
Newly hatched domestic chicks serve as an important model for experimental studies of neural and behavioral plasticity. Brain-derived neurotrophic factor (BDNF) has been shown to play a critical role in synaptic plasticity, including long-term potentiation, which underlies learning and memory in rodents. Here we show that BDNF mRNA levels increased in the intermediate medial hyperpallium apicale (IMHA), which is the caudal area of the visual Wulst, of imprinted chick brains, and the upregulation of gene expression correlated with the strength of the learned preference to the training object. In addition, activation of tropomyosin-related kinase B (TrkB)/phosphatidylinositol 3-kinase signaling was associated with filial imprinting. However, pharmacological deprivation of TrkB phosphorylation in IMHA did not impair memory formation, suggesting that activation of BDNF/TrkB signaling in IMHA is not involved in memory acquisition in filial imprinting.
新孵化的家鸡是神经和行为可塑性实验研究的重要模型。脑源性神经营养因子(BDNF)已被证明在突触可塑性中起关键作用,包括长期增强,这是啮齿动物学习和记忆的基础。在这里,我们表明,在印记鸡脑的视觉顶叶中间内侧顶叶(IMHA)中,BDNF mRNA水平升高,IMHA是视觉顶叶的尾侧区域,基因表达的上调与对训练对象的学习偏好强度相关。此外,原肌球蛋白相关激酶B(TrkB)/磷脂酰肌醇3激酶信号的激活与亲子印记有关。然而,可以IMHA中TrkB磷酸化的药理学剥夺不会损害记忆形成,这表明IMHA中BDNF/TrkB信号的激活不参与亲子印记中的记忆获取。