M. H. MONFILS1, J. DEBIEC1, *G. E. SCHAFE2, J. E. LEDOUX1, V. DOYERE3;
1Center for Neural Science, New York University, New York, NY, 2Psychology, Yale University, New Haven, CT, 3NAMC, Universite Paris-Sud, Paris, FRANCE.

When a neutral stimulus, such as tone, is paired with a noxious stimulus, such as footshock, it acquires the ability to elicit fear responses through a Pavlovian associative learning process. Fear memories, once consolidated in a long-term stable state, are, when reactivated, updated through a reconsolidation process. Considerable evidence indicates that the lateral amygdala (LA) is critical for the initial storage and reconsolidation of auditory fear memories. Recently, we have shown that the reconsolidation process in the amygdala is specific to the cue that is reactivated (Debiec et al., 2006). Auditory signals reach the LA from areas of the thalamus and cortex. The present experiments examined the role of thalamic input synapses in the reconsolidation process. Rats were chronically implanted with bilateral cannulae in the LA, a recording electrode attached to the left cannula, and a stimulating electrode in the left auditory thalamus (MGm/PIN). Rats were then submitted to a training protocol in which two tones (1 kHz, 50 ms pips; FM sweeps, 10-15 kHz, 250 ms) were used. Rats were habituated, conditioned, and reactivated to one of the tones. Following reactivation, rats were tested for fear retention both at 3hr and ~24h later. Behavioral (freezing) and short-latency neurophysiological responses (field potentials in the LA and in the MGM/PIN) evoked by each of the tones were recorded and analysed during each phase of the experiment. The effects of intra-LA infusion of pharmacological agents known to disrupt the reconsolidation process were compared (MAP kinase inhibitor, U0126 and beta-adrenergic antagonist, propanolol). We found a selective deficit in memory for the tone reactivated in the presence of U0126. This selective behavioral deficit was accompanied by a long-term, but not a short-term, decrease in the potentiation of neurophysiological responses in the LA evoked by that same cue. Further, neural responses evolved by both stimuli were unaffected in the MGm/PIN. The question of whether propanolol produces the same pattern of results is under investigation. These results indicate that thalamic input synapse plasticity in LA is involved in the reconsolidation of auditory fear memories in a cue-specific manner. Further, the results indicate that the thalamic path is able to store relatively specific information about the stimulus.
Support Contributed By: CNRS-PICS;NSERC;AHFMR;VW I/79 894;NIH MH067048, MH046516, MH38774

Program No. 370.3/KK21
Poster presentation:Monday, Oct 16, 2006, 10:00 AM -11:00 AM
Location: Georgia World Congress Center: Halls B3-B5