Fear conditioning induces associative long-term potentiation in the amygdala

M. T. Rogan, U. V. Staubli, Joseph Ledoux

Research output: Contribution to journalArticle

Abstract

Long-term potentiation (LTP) is an experience-dependent form of neural plasticity believed to involve mechanisms that underlie memory formation. LTP has been studied most extensively in the hippocampus, but the relation between hippocampal LTP and memory has been difficult to establish. Here we explore the relation between LTP and memory in fear conditioning, an amygdala-dependent form of learning in which an innocuous conditioned stimulus (CS) elicits fear responses after being associatively paired with an aversive unconditioned stimulus (US). We have previously shown that LTP induction in pathways that transmit auditory CS information to the lateral nucleus of the amygdala (LA) increases auditory-evoked field potentials in this nucleus. Now we show that fear conditioning alters auditory CS-evoked responses in LA in the same way as LTP induction. The changes parallel the acquisition of CS-elicited fear behaviour, are enduring, and do not occur if the CS and US remain unpaired. LTP-like associative processes thus occur during fear conditioning, and these may underlie the long-term associative plasticity that constitutes memory of the conditioning experience.

Original languageEnglish (US)
Pages (from-to)604-607
Number of pages4
JournalNature
Volume390
Issue number6660
DOIs
StatePublished - 1997

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Long-Term Potentiation
Amygdala
Fear
Long-Term Memory
Auditory Pathways
Auditory Evoked Potentials
Neuronal Plasticity
Conditioning (Psychology)
Hippocampus
Learning

ASJC Scopus subject areas

  • General

Cite this

Fear conditioning induces associative long-term potentiation in the amygdala. / Rogan, M. T.; Staubli, U. V.; Ledoux, Joseph.

In: Nature, Vol. 390, No. 6660, 1997, p. 604-607.

Research output: Contribution to journalArticle

Rogan, M. T. ; Staubli, U. V. ; Ledoux, Joseph. / Fear conditioning induces associative long-term potentiation in the amygdala. In: Nature. 1997 ; Vol. 390, No. 6660. pp. 604-607.
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