Asymmetries in long-term and short-term plasticity at thalamic and cortical inputs to the amygdala in vivo

Authors

  • Torfi Sigurðsson,

    1. Center for Neural Science, New York University, 4 Washington Place, New York, NY 10003, USA
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    • *

      Present address: Department of Psychiatry, Columbia University, Unit 87 P.I. Annex L144, 1051 Riverside Drive, New York, NY 10032, USA

  • Christopher K. Cain,

    1. Center for Neural Science, New York University, 4 Washington Place, New York, NY 10003, USA
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  • Valérie Doyère,

    1. Center for Neural Science, New York University, 4 Washington Place, New York, NY 10003, USA
    2. CNRS, UMR8620, NAMC, Orsay, France
    3. Université Paris-Sud, UMR8620, Orsay, France
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  • Joseph E. LeDoux

    1. Center for Neural Science, New York University, 4 Washington Place, New York, NY 10003, USA
    2. Nathan Kline Institute for Psychiatric Research, Orangeburg, NY, USA
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Errata

This article is corrected by:

  1. Errata: Asymmetries in long-term and short-term plasticity at thalamic and cortical inputs to the amygdala in vivo Volume 31, Issue 5, 950, Article first published online: 22 February 2010

Dr T. Sigurðsson, at *present address below.
E-mail: ts2414@columbia.edu

Abstract

Converging lines of evidence suggest that synaptic plasticity at auditory inputs to the lateral amygdala (LA) is critical for the formation and storage of auditory fear memories. Auditory information reaches the LA from both thalamic and cortical areas, raising the question of whether they make distinct contributions to fear memory storage. Here we address this by comparing the induction of long-term potentation (LTP) at the two inputs in vivo in anesthetized rats. We first show, using field potential measurements, that different patterns and frequencies of high-frequency stimulation (HFS) consistently elicit stronger LTP at cortical inputs than at thalamic inputs. Field potential responses elicited during HFS of thalamic inputs were also smaller than responses during HFS of cortical inputs, suggesting less effective postsynaptic depolarization. Pronounced differences in the short-term plasticity profiles of the two inputs were also observed: whereas cortical inputs displayed paired-pulse facilitation, thalamic inputs displayed paired-pulse depression. These differences in short- and long-term plasticity were not due to stronger inhibition at thalamic inputs: although removal of inhibition enhanced responses to HFS, it did not enhance thalamic LTP and left paired-pulse depression unaffected. These results highlight the divergent nature of short- and long-term plasticity at thalamic and cortical sensory inputs to the LA, pointing to their different roles in the fear learning system.

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