Why We Think Plasticity Underlying Pavlovian Fear Conditioning Occurs in the Basolateral Amygdala

The encoding view provides a parsimonious account of the multiple convergent lines of evidence for the ABL’s role in fear conditioning. We do not dispute the notion that activation of the ABL can facilitate consolidation of information in other structures, such as the hippocampus, other cortical areas, or the striatum (4xMechanisms of emotional arousal and lasting declarative memory. Cahill, L and McGaugh, J.L. Trends Neurosci. 1998; 21: 294–299Abstract | Full Text | Full Text PDF | PubMed | Scopus (952)See all References, 27xAmygdala modulation of multiple memory systems (hippocampus and caudate-putamen) . Packard, M.G and Teather, L.A. Neurobiol. Learn. Mem. 1998; 69: 163–203Crossref | PubMed | Scopus (214)See all References). Rather, we argue that the ABL is involved in the encoding of fear memory and the modulation of memory functions of other structures.While we believe that the ABL is essential to the implicit learning that constitutes fear conditioning, we are not proposing that all of the plasticity relevant to fear conditioning necessarily occurs within the ABL. It seems possible that the ABL, while essential, is also part of a distributed network that encodes the fear memory. For example, as noted, there is compelling evidence that plastic changes occur in regions that are afferent to the ABL, such as thalamic and cortical sensory systems that process CSs (see Weinberger 1995xRetuning the brain by fear conditioning. Weinberger, N.M. See all ReferencesWeinberger 1995). Additionally, cortical areas that are both afferent and efferent to the ABL (e.g., perirhinal cortex, the hippocampal formation, and sensory cortex) may participate with the ABL in the long-term encoding of fear. It remains for future research to determine whether these distributed representations exist and, if so, to unravel their nature.‡To whom correspondence should be addressed (e-mail: fanselow@ucla.edu).

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