Effects of stress on AMPA receptor distribution and function in the basolateral amygdala

• Type of Material: Article
• Authors: Donald Rainnie, Emory University; E. Muly, Emory University; GW Hubert, Atlanta Veteran’s Medical Center; C Li, Yerkes National Primate Research Center
• Language: English
• Date: 2014-07-01
• Publisher: Springer (part of Springer Nature): Springer Open Choice Hybrid Journals
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2013 Springer-Verlag.
• Final Published Version (URL): http://dx.doi.org/10.1007/s00429-013-0557-z
• Title of Journal or Parent Work: Brain Structure and Function
• ISSN: 1863-2653
• Volume: 219
• Issue: 4
• Start Page: 1169
• End Page: 1179
• Grant/Funding Information: This work was supported by a Merit Award from the Office of Research and Development, Department of Veterans Affairs to ECM; by NIMH grant MH069852 to DGR; and by an NIH/NCRR base grant [Grant P51RR000165] to Yerkes National Primate Research Center.
• Keywords: Neurosciences & Neurology; DISORDER; Anatomy & Morphology; ANXIETY; Life Sciences & Biomedicine; VISUAL-CORTEX; FEAR MEMORIES; LONG-TERM POTENTIATION; GluR1; RAT AMYGDALA; LTP; Stress; SYNAPTIC PLASTICITY; LATERAL AMYGDALA; MEMORY FORMATION; Science & Technology; Basolateral amygdala; SYNAPSES; Neurosciences
• Research Categories: Biology, Animal Physiology; Biology, Anatomy; Biology, Neuroscience

Abstract

Stress is a growing public health concern and can lead to significant disabilities. The neural response to stressors is thought to be dependent on the extended amygdala. The basolateral amygdala (BLA) is responsible for associations of sensory stimuli with emotional valence and is thought to be involved in stress-induced responses. Previous behavioral and electrophysiological experiments demonstrate that, in response to stress, changes occur in glutamatergic neurotransmission within the BLA and, in particular in transmission at AMPA receptors. Given the established role of AMPA receptors in memory and synaptic plasticity, we tested the hypothesis that stress produces alterations in the distribution of these receptors in a way that might account for stress-induced alterations in amygdala circuitry function. We examined the subcellular localization of GluR1 subunits of the AMPA receptor and the electrophysiological characteristics of BLA principal neurons in an animal model of unpredictable stress. Compared to controls, we demonstrated an increase in the ratio of labeled spines to labeled dendritic shafts in the BLA of rats 6 and 14 days post-stress, but not 1 day post-stress. Furthermore, the frequency of mini-EPSCs was increased in stressed animals without a change in general membrane properties, mini-EPSC amplitude, or in paired pulse modulation of glutamate release. Taken together, these data suggest that the shift of GluR1-containing AMPA receptors from dendritic stores into spines may be in part responsible for the persistent behavioral alterations observed following severe stressors.