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Role of AMPA receptor trafficking in NMDA receptor‐dependent synaptic plasticity in the rat lateral amygdala
Author(s) -
Yu Shu Yan,
Wu Dong Chuan,
Liu Lidong,
Ge Yuan,
Wang Yu Tian
Publication year - 2008
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/j.1471-4159.2008.05461.x
Subject(s) - long term potentiation , ampa receptor , synaptic plasticity , long term depression , nmda receptor , neuroscience , synaptic fatigue , glutamate receptor , synaptic augmentation , chemistry , biology , microbiology and biotechnology , receptor , biochemistry
Stimulated exocytosis and endocytosis of post‐synaptic α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid subtype of glutamate receptors (AMPARs) have been proposed as primary mechanisms for the expression of hippocampal CA1 long‐term potentiation (LTP) and long‐term depression (LTD), respectively. LTP and LTD, the two most well characterized forms of synaptic plasticity, are thought to be important for learning and memory in behaving animals. Both LTP and LTD can also be induced in the lateral amygdala (LA), a critical structure involved in fear conditioning. However, the role of AMPAR trafficking in the expression of either LTP or LTD in this structure remains unclear. In this study, we show that NMDA receptor‐dependent LTP and LTD can be reliably induced at the synapses of the auditory thalamic inputs to the LA in brain slices. The expression of LTP was prevented by post‐synaptic blockade of vesicle‐mediated exocytosis with application of a light chain of Clostridium tetanus neurotoxin and was associated with increased cell‐surface AMPAR expression. In contrast, the expression of LTD was prevented by post‐synaptic application of a glutamate receptor 2‐derived interference peptide, which specifically blocks the stimulated clathrin‐dependent endocytosis of AMPARs, and was correlated with a reduction in plasma membrane‐surface expression of AMPARs. These results strongly suggest that regulated trafficking of post‐synaptic AMPARs is also involved in the expression of LTP and LTD in the LA.