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Positive feedback of NR 2B‐containing NMDA receptor activity is the initial step toward visual imprinting: a model for juvenile learning
Author(s) -
Nakamori Tomoharu,
Sato Katsushige,
Kinoshita Masae,
Kanamatsu Tomoyuki,
Sakagami Hiroyuki,
Tanaka Kohichi,
OhkiHamazaki Hiroko
Publication year - 2015
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/jnc.12954
Subject(s) - imprinting (psychology) , nmda receptor , long term potentiation , biology , neuroscience , gene knockdown , synaptic plasticity , microbiology and biotechnology , chemistry , receptor , biochemistry , gene , apoptosis
Imprinting in chicks is a good model for elucidating the processes underlying neural plasticity changes during juvenile learning. We recently reported that neural activation of a telencephalic region, the core region of the hyperpallium densocellulare ( HDC o), was critical for success of visual imprinting, and that N‐Methyl‐D‐aspartic ( NMDA ) receptors containing the NR 2B subunit ( NR 2B/ NR 1) in this region were essential for imprinting. Using electrophysiological and multiple‐site optical imaging techniques with acute brain slices, we found that long‐term potentiation ( LTP ) and enhancement of NR 2B/ NR 1 currents in HDC o neurons were induced in imprinted chicks. Enhancement of NR 2B/ NR 1 currents as well as an increase in surface NR 2B expression occurred even following a brief training that was too weak to induce LTP or imprinting behavior. This means that NR 2B/ NR 1 activation is the initial step of learning, well before the activation of alpha‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate receptors which induces LTP . We also showed that knockdown of NR 2B/ NR 1 inhibited imprinting, and inversely, increasing the surface NR 2B expression by treatment with a casein kinase 2 inhibitor successfully reduced training time required for imprinting. These results suggest that imprinting stimuli activate post‐synaptic NR 2B/ NR 1 in HDC o cells, increase NR 2B/ NR 1 signaling through up‐regulation of its expression, and induce LTP and memory acquisition.The study investigated the neural mechanism underlying juvenile learning. In the initial stage of chick imprinting, NMDA receptors containing the NMDA receptor subunit 2B (NR2B) are activated, surface expression of NR2B/NR1 (NMDA receptor subunit 1) is up‐regulated, and consequently long‐term potentiation is induced in the telencephalic neurons. We suggest that the positive feedback in the NR2B/NR1 activation is a unique process of juvenile learning, exhibiting rapid memory acquisition.