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Received for publication July 25, 2005.
Revised October 3, 2005.
Accepted for publication October 7, 2005.
Fear conditioning has been ascribed to presynaptic mechanisms, particularly presynaptic facilitation of transmission at thalamo- and cortico-amygdala synapses. Here by labeling surface receptors with biotin or using membrane fractionation approaches, we reported that fear conditioning resulted in an increase in surface expression of GluR1 subunit of AMPA receptors in the amygdala whereas total GluR1 mRNA and protein levels were unchanged. The control group that received conditioned stimulus (CS) and unconditioned stimulus (US) in an unpaired fashion did not present any increase, indicating that GluR1 increase was specific to the learning component of the task. Conditioning-induced increase in surface expression of GluR1 depended on the activation of NMDA receptors and protein kinases, and required synthesis of new proteins. CS-alone trials applied at 24 hr before training attenuated fear-potentiated startle and prevented conditioning-induced increase in surface expression of GluR1. Increase in GluR1 was also observed in the amygdala slices after delivery of tetanic stimulation (TS) that elicited long-term potentiation (LTP) of synaptic transmission. Proteasome inhibitor increased surface expression of GluR1 in a time- and dose-dependent manner. Furthermore, pre-training administration of proteasome inhibitor into the amygdala facilitated fear-potentiated startle. These results suggest that long-term memory formation is correlated with the change in synaptic expression of GluR1 and trafficking of GluR1 to the synaptic sites contributes at least in part to the expression of fear memory.
Key words:
Glutamate, Protein Kinases (other), Receptor synthesis/trafficking, Recycling, Synaptic plasticity
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