LeDoux Lab 2005 SfN Abstracts

LOCAL SYNAPTIC PLASTICITY IS REQUIRED FOR LONG-TERM STORAGE OF A FEAR MEMORY IN THE LATERAL AMYGDALA V.Doyere1*; J.M.Edeline1*; J.E.LeDoux2; G.E.Schafe3 1. NAMC, CNRS, UMR 8620, Univ. Paris Sud, Orsay, France 2. Center for Neural Science, NYU, New York, NY, USA 3. Psychology, Yale Univ., New Haven, CT, USA Auditory fear conditioning leads to alterations in the activity of LA neurons, presumably reflecting plasticity at LA synapses (Fanselow & LeDoux, 1999). However, cells within the auditory thalamus (MGm/PIN), like those in LA, rapidly develop increased firing to the conditioned stimulus with fear conditioning. This pattern of findings has supported the argument that the plasticity observed in the LA after fear conditioning might merely be a reflection of plastic changes that have occurred in the MGm/PIN (Cahill et al, 1999). To directly address the question of whether neurophysiological changes in the LA induced by fear conditioning are of local origin, we combined electrophysiological recordings in freely behaving rats with intra-LA infusion of an inhibitor of ERK/MAP kinase, a pharmacological treatment that impairs memory consolidation of auditory fear conditioning. Rats were implanted with cannulae aimed bilaterally at the LA and recording electrodes into both LA and MGm/PIN. Before conditioning, rats received intra-LA infusion of U0126 (an inhibitor of MEK, an upstream regulator of ERK/MAP kinase; 1 g/side) or 50% DMSO vehicle. Both short-term memory (STM) and long-term memory (LTM) of auditory fear conditioning were tested, and auditory-evoked responses were recorded simultaneously from both LA and MGm/PIN. As expected, local inhibition of ERK/MAPK in the LA impaired LTM, but not STM of auditory fear conditioning. Importantly, local infusion of U0126 impaired long-term, but not short-term, retention of conditioning-induced enhancements of auditory-evoked responses in the LA, while having no effect on those in MGm/PIN. These findings strongly suggest that auditory fear memories are not passively transmitted from the thalamus but instead require synaptic plasticity within the LA. Support Contributed By: NIMH grants MH46516, MH067048, MH38774 (to J.E.L), CNRS-NSF17089 (to V.D. and J.E.L.), and NIMH grant MH62519 (to G.E.S). Program No. 415.1 Poster presentation:Monday, Nov. 14, 8:00 AM - 9:00 AM Location: HH24