| THE AUDITORY THALAMUS CONTRIBUTES TO MEMORY FORMATION
OF AUDITORY FEAR CONDITIONING VIA THE ERK/MAP KINASE SIGNALING PATHWAY
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| A.M. Schoute; J.-S. Choi*; J.E. LeDoux
G.E. Schafe |
| Center for Neural Science, New York University, New York,
NY, USA |
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Auditory fear conditioning
involves transmission of sensory information to the lateral nucleus
of the amygdala (LA), where alterations in synaptic transmission are
thought to play a key role in memory formation and storage. It has
been known for some time, however, that the auditory thalamus (MGm/PIN),
which lies upstream from the LA, also undergoes associative neuronal
plasticity during auditory fear conditioning. However, the functional
significance of this thalamic plasticity remains unknown. In the present
study, we evaluated the role of protein synthesis and the mitogen-activated
protein kinase (ERK/MAPK) signaling pathway in the MGm/PIN in auditory
fear conditioning. In the first series of experiments, rats were given
infusions of U0126 (1.0 or 0.1  g/side),
which blocks MEK, an upstream regulator of ERK/MAPK , into the MGm/PIN
prior to auditory Pavlovian fear conditioning. Findings showed that
long-term memory (LTM; at 24 Hr) was dose-dependently impaired, while
short-term memory (STM; at 1, 3, or 6 Hr) was intact. In the second
series of experiments, rats were given intra-MGm/PIN infusions of
U0126 (1.0 g) or multiple doses
of the protein synthesis inhibitor anisomycin (62.5 or 125 g/side) immediately after
single-trial fear conditioning. As in the initial experiments, infusion
of U0126 significantly impaired retention of auditory fear conditioning
(24 Hr later). However, infusion of anisomycin had no effect at either
dose. Together, these results suggest the intriguing possibility that
the MGN/PIN contributes to memory formation, but is not itself a site
of storage, of Pavlovian fear conditioning.
Supported by: MH38774 & MH62519
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