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Fear memories induce a switch in stimulus response and signaling mechanisms for long-term potentiation in the lateral amygdala.
Eur J Neurosci. 2004 Jul; 20(2):549-56.EJ

Abstract

Activity-dependent modification of synapses is fundamental for information storage in the brain and underlies behavioral learning. Fear conditioning is a model of emotional memory and anxiety that is expressed as an enduring increase in synaptic strength in the lateral amygdala (LA). Here we analysed synaptic plasticity in the rat cortico-LA pathway during maintenance of fear memory. We show for the first time that the stimulus frequency for synaptic potentiation is switched during maintenance of fear memory, and the underlying signaling mechanisms are altered in the cortico-LA pathway. In slices from fear-conditioned animals, high-frequency stimulation-induced (HFS) long-term potentiation (LTP) was attenuated, whereas low-frequency stimulation (LFS) elicited a long-lasting potentiation. HFS generates robust LTP that is dependent on N-methyl-d-aspartate receptor (NMDAR) and L-type voltage-gated calcium channel (VGCC) activation in control animals, whereas in fear-conditioned animals HFS LTP is NMDAR- and VGCC-independent. LFS-LTP is partially NMDAR-dependent, but VGCCs are necessary for potentiation in fear memory. Collectively, these results show that during maintenance of fear memory the stimulus requirements for amygdala afferents and critical signaling mechanisms for amygdala synaptic potentiation are altered, suggesting that cue-engaged synaptic mechanisms in the amygdala are dramatically affected as a result of emotional learning.

Authors+Show Affiliations

Department of Pharmacology and Toxicology, The University of Texas Medical Branch, 301 University Blvd., Galveston, Texas, 77555-1031, USA. bwschroe@utmb.eduNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15233764

Citation

Schroeder, Bradley W., and Patricia Shinnick-Gallagher. "Fear Memories Induce a Switch in Stimulus Response and Signaling Mechanisms for Long-term Potentiation in the Lateral Amygdala." The European Journal of Neuroscience, vol. 20, no. 2, 2004, pp. 549-56.
Schroeder BW, Shinnick-Gallagher P. Fear memories induce a switch in stimulus response and signaling mechanisms for long-term potentiation in the lateral amygdala. Eur J Neurosci. 2004;20(2):549-56.
Schroeder, B. W., & Shinnick-Gallagher, P. (2004). Fear memories induce a switch in stimulus response and signaling mechanisms for long-term potentiation in the lateral amygdala. The European Journal of Neuroscience, 20(2), 549-56.
Schroeder BW, Shinnick-Gallagher P. Fear Memories Induce a Switch in Stimulus Response and Signaling Mechanisms for Long-term Potentiation in the Lateral Amygdala. Eur J Neurosci. 2004;20(2):549-56. PubMed PMID: 15233764.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Fear memories induce a switch in stimulus response and signaling mechanisms for long-term potentiation in the lateral amygdala. AU - Schroeder,Bradley W, AU - Shinnick-Gallagher,Patricia, PY - 2004/7/6/pubmed PY - 2004/10/1/medline PY - 2004/7/6/entrez SP - 549 EP - 56 JF - The European journal of neuroscience JO - Eur J Neurosci VL - 20 IS - 2 N2 - Activity-dependent modification of synapses is fundamental for information storage in the brain and underlies behavioral learning. Fear conditioning is a model of emotional memory and anxiety that is expressed as an enduring increase in synaptic strength in the lateral amygdala (LA). Here we analysed synaptic plasticity in the rat cortico-LA pathway during maintenance of fear memory. We show for the first time that the stimulus frequency for synaptic potentiation is switched during maintenance of fear memory, and the underlying signaling mechanisms are altered in the cortico-LA pathway. In slices from fear-conditioned animals, high-frequency stimulation-induced (HFS) long-term potentiation (LTP) was attenuated, whereas low-frequency stimulation (LFS) elicited a long-lasting potentiation. HFS generates robust LTP that is dependent on N-methyl-d-aspartate receptor (NMDAR) and L-type voltage-gated calcium channel (VGCC) activation in control animals, whereas in fear-conditioned animals HFS LTP is NMDAR- and VGCC-independent. LFS-LTP is partially NMDAR-dependent, but VGCCs are necessary for potentiation in fear memory. Collectively, these results show that during maintenance of fear memory the stimulus requirements for amygdala afferents and critical signaling mechanisms for amygdala synaptic potentiation are altered, suggesting that cue-engaged synaptic mechanisms in the amygdala are dramatically affected as a result of emotional learning. SN - 0953-816X UR - https://www.unboundmedicine.com/medline/citation/15233764/Fear_memories_induce_a_switch_in_stimulus_response_and_signaling_mechanisms_for_long_term_potentiation_in_the_lateral_amygdala_ DB - PRIME DP - Unbound Medicine ER -