Activation of brain-derived neurotrophic factor/tropomyosin-related kinase B signaling accompanying filial imprinting in domestic chicks (Gallus gallus domesticus).
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.
Faculty of Pharmaceutical Sciences, Teikyo University, Kaga, Itabashi-ku, Tokyo, Japan.
Shinji
S
Yamaguchi
Naoya
N
Aoki
Daisuke
D
Kobayashi
Takaaki
T
Kitajima
Eiji
E
Iikubo
Sachiko
S
Katagiri
Toshiya
T
Matsushima
Koichi J
KJ
Homma
D000818:Animals; D019208:Brain-Derived Neurotrophic Factor / Q000235:genetics*; D002645:Chickens / Q000502:physiology*; D007173:Imprinting, Psychological / Q000502:physiology*; D020813:Receptor, trkB / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*; D013687:Telencephalon / Q000254:growth & development / Q000378:metabolism*
D019208:Brain-Derived Neurotrophic Factor; D020813:Receptor, trkB