Kainate receptor-mediated heterosynaptic facilitation in the amygdala

He Li, Aiqin Chen, Guoqiang Xing, Mei Ling Wei, Michael A Rogawski

Research output: Contribution to journalArticle

83 Citations (Scopus)

Abstract

Prolonged low-frequency stimulation of excitatory afferents to basolateral amygdala neurons results in enduring enhancement of excitatory synaptic responses. The induction of this form of synaptic plasticity is eliminated by selective antagonists of GluR5 kainate receptors and can be mimicked by the GluR5 agonist ATPA. Kainate receptor-mediated synaptic facilitation generalizes to include inactive afferent synapses on the target neurons, and therefore contrasts with other types of activity-dependent enduring synaptic facilitation that are input-pathway specific. Such heterosynaptic spread of synaptic facilitation could account for adaptive and pathological expansion in the set of critical internal and external stimuli that trigger amygdala-dependent behavioral responses.

Original languageEnglish (US)
Pages (from-to)612-620
Number of pages9
JournalNature Neuroscience
Volume4
Issue number6
DOIs
StatePublished - 2001
Externally publishedYes

Fingerprint

Kainic Acid Receptors
Amygdala
Neurons
Neuronal Plasticity
Synapses
Gluk1 kainate receptor
Basolateral Nuclear Complex

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Kainate receptor-mediated heterosynaptic facilitation in the amygdala. / Li, He; Chen, Aiqin; Xing, Guoqiang; Wei, Mei Ling; Rogawski, Michael A.

In: Nature Neuroscience, Vol. 4, No. 6, 2001, p. 612-620.

Research output: Contribution to journalArticle

Li, He ; Chen, Aiqin ; Xing, Guoqiang ; Wei, Mei Ling ; Rogawski, Michael A. / Kainate receptor-mediated heterosynaptic facilitation in the amygdala. In: Nature Neuroscience. 2001 ; Vol. 4, No. 6. pp. 612-620.
@article{c0413bf256c440f3a9dc6c9d4248270d,
title = "Kainate receptor-mediated heterosynaptic facilitation in the amygdala",
abstract = "Prolonged low-frequency stimulation of excitatory afferents to basolateral amygdala neurons results in enduring enhancement of excitatory synaptic responses. The induction of this form of synaptic plasticity is eliminated by selective antagonists of GluR5 kainate receptors and can be mimicked by the GluR5 agonist ATPA. Kainate receptor-mediated synaptic facilitation generalizes to include inactive afferent synapses on the target neurons, and therefore contrasts with other types of activity-dependent enduring synaptic facilitation that are input-pathway specific. Such heterosynaptic spread of synaptic facilitation could account for adaptive and pathological expansion in the set of critical internal and external stimuli that trigger amygdala-dependent behavioral responses.",
author = "He Li and Aiqin Chen and Guoqiang Xing and Wei, {Mei Ling} and Rogawski, {Michael A}",
year = "2001",
doi = "10.1038/88432",
language = "English (US)",
volume = "4",
pages = "612--620",
journal = "Nature Neuroscience",
issn = "1097-6256",
publisher = "Nature Publishing Group",
number = "6",

}

TY - JOUR

T1 - Kainate receptor-mediated heterosynaptic facilitation in the amygdala

AU - Li, He

AU - Chen, Aiqin

AU - Xing, Guoqiang

AU - Wei, Mei Ling

AU - Rogawski, Michael A

PY - 2001

Y1 - 2001

N2 - Prolonged low-frequency stimulation of excitatory afferents to basolateral amygdala neurons results in enduring enhancement of excitatory synaptic responses. The induction of this form of synaptic plasticity is eliminated by selective antagonists of GluR5 kainate receptors and can be mimicked by the GluR5 agonist ATPA. Kainate receptor-mediated synaptic facilitation generalizes to include inactive afferent synapses on the target neurons, and therefore contrasts with other types of activity-dependent enduring synaptic facilitation that are input-pathway specific. Such heterosynaptic spread of synaptic facilitation could account for adaptive and pathological expansion in the set of critical internal and external stimuli that trigger amygdala-dependent behavioral responses.

AB - Prolonged low-frequency stimulation of excitatory afferents to basolateral amygdala neurons results in enduring enhancement of excitatory synaptic responses. The induction of this form of synaptic plasticity is eliminated by selective antagonists of GluR5 kainate receptors and can be mimicked by the GluR5 agonist ATPA. Kainate receptor-mediated synaptic facilitation generalizes to include inactive afferent synapses on the target neurons, and therefore contrasts with other types of activity-dependent enduring synaptic facilitation that are input-pathway specific. Such heterosynaptic spread of synaptic facilitation could account for adaptive and pathological expansion in the set of critical internal and external stimuli that trigger amygdala-dependent behavioral responses.

UR - http://www.scopus.com/inward/record.url?scp=0034990330&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034990330&partnerID=8YFLogxK

U2 - 10.1038/88432

DO - 10.1038/88432

M3 - Article

VL - 4

SP - 612

EP - 620

JO - Nature Neuroscience

JF - Nature Neuroscience

SN - 1097-6256

IS - 6

ER -