*J. P. LITTLE, N. HARANHALLI, L. W. MASSIE, J. E. LEDOUX, L. R. JOHNSON;
Ctr. for Neural Sci., New York Univ., New York, NY

The acquisition of Pavlovian fear-memories depends upon neural plasticity in the lateral amygdala (LA). During conditioning, rats learn to associate a naturally aversive, unconditioned stimulus (US) with a neutral, conditioned stimulus (CS) when they are temporally paired. Evidence suggests that upon memory recall, CS induced activation of the memory trace in LA recruits the central nucleus of the amygdala, the principle output nucleus. Recent work, however, suggests that other amygdala nuclei, in particular the central nucleus (Ce), may also undergo learning-related plasticity during memory acquisition. Functional inactivation disrupts memory acquisition, suggesting the central may actively encode associative information (Wilensky et al. 2006). In addition, recent models indicate that cells in the central nucleus can undergo plasticity at the thalamo-amydalar pathway (Pare et al. 2004). Taken together, these results indicate that the central amygdala does not merely act as an output nucleus, but encodes elements of the associate memory as well. We used Pavlovian fear conditioning to further investigate synaptic plasticity in each subnucleus of the central and basal amygdala. Rats were subjected to 5 paired presentations of the CS (20sec, 5kHz, 75db tone) and US (0.5sec, 1.0mA foot shock), and control rats received the same stimuli in an unpaired fashion. Brains were then prepared for immunocytochemical detection of phosphorylated mitogen activated kinase (pMAPK), a chemical marker for neuronal plasticity (Schafe et al 2000). We counted all labeled neurons in the central and basal amygdala using a light microscope equipped with Neurolucida (Microbrightfield, VT). In contrast to previous results from LA (Schafe, et al. 2000; LeDoux et al. 2006 SFN abstracts), our results do not indicate a significant increase in the number of pMAPK labeled neurons in any Central or Basal subnucleus, in the rats which received paired stimuli. These initial data suggest that neither the central nor the basal amygdala show cellular changes as a result of Pavlovian fear conditioning. However, the dense presence of pMAPK neurons in the Central nucleus suggests that some plasticity is occurring in this nucleus which may be triggered by learning independent to US and CS pairing.

Support Contributed By:NIH grant R01 MH46516;NIH grant R37 MH38774;NIH grant K05 MH067048;NIH grantsP50 MH58911



Program No. 307.1/BBB14
Poster presentation:Sunday, Nov 04, 2007, 1:00 PM - 2:00 PM
Location: San Diego Convention Center: Halls B-H