Amygdala upregulation of NCAM polysialylation induced by auditory fear conditioning is not required for memory formation, but plays a role in fear extinction.
Neurobiology of Learning and Memory. 2007-05-01; 87(4): 573-582
DOI: 10.1016/j.nlm.2006.11.007
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1. Neurobiol Learn Mem. 2007 May;87(4):573-82. Epub 2007 Jan 12.
Amygdala upregulation of NCAM polysialylation induced by auditory fear
conditioning is not required for memory formation, but plays a role in fear
extinction.
Markram K(1), Lopez Fernandez MA, Abrous DN, Sandi C.
Author information:
(1)Brain Mind Institute, Ecole Polytechnique Fédérale de Lausanne, Switzerland.
There is much interest to understand the mechanisms leading to the establishment,
maintenance, and extinction of fear memories. The amygdala has been critically
involved in the processing of fear memories and a number of molecular changes
have been implicated in this brain region in relation to fear learning. Although
neural cell adhesion molecules (NCAMs) have been hypothesized to play a role,
information available about their contribution to fear memories is scarce. We
investigate here whether polysialylated NCAM (PSA-NCAM) contributes to auditory
fear conditioning in the amygdala. First, PSA-NCAM expression was evaluated in
different amygdala nuclei after auditory fear conditioning at two different shock
intensities. Results showed that PSA-NCAM expression was increased 24 h
post-training only in animals subjected to the highest shock intensity (1mA).
Second, PSA-NCAM was cleaved in the basolateral amygdaloid complex through
micro-infusions of the enzyme endoneuraminidase N, and the consequences of such
treatment were investigated on the acquisition, consolidation, remote memory
expression, and extinction of conditioned fear memories. Intra-amygdaloid
cleavage of PSA-NCAM did not affect acquisition, consolidation or expression of
remote fear memories. However, intra-amygdaloid PSA-NCAM cleavage enhanced fear
extinction processes. These results suggest that upregulation of PSA-NCAM is a
correlate of fear conditioning that is not necessary for the establishment of
fear memory in the amygdala, but participates in mechanisms precluding fear
extinction. These findings point out PSA-NCAM as a potential target for the
treatment of psychopathologies that involve impairment in fear extinction.
DOI: 10.1016/j.nlm.2006.11.007
PMID: 17223582 [Indexed for MEDLINE]