Neuronal signaling of fear memory. Nature Reviews

Department of Psychology and Neuroscience Program, University of Michigan, Ann Arbor, Michigan 48109, USA.
Nature reviews Neuroscience (Impact Factor: 31.43). 12/2004; 5(11):844-52. DOI: 10.1038/nrn1535
Source: PubMed


The learning and remembering of fearful events depends on the integrity of the amygdala, but how are fear memories represented in the activity of amygdala neurons? Here, we review recent electrophysiological studies indicating that neurons in the lateral amygdala encode aversive memories during the acquisition and extinction of Pavlovian fear conditioning. Studies that combine unit recording with brain lesions and pharmacological inactivation provide evidence that the lateral amygdala is a crucial locus of fear memory. Extinction of fear memory reduces associative plasticity in the lateral amygdala and involves the hippocampus and prefrontal cortex. Understanding the signalling of aversive memory by amygdala neurons opens new avenues for research into the neural systems that support fear behaviour.

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Available from: Stephen Maren, Oct 08, 2015
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    • "The ventral hippocampus (vHPC) and the basolateral amygdala (BLA) are part of an extensive neural circuit encoding emotional memories (Fanselow, 2010; Maren and Quirk, 2004). This circuit can be dysfunctional in neuropsychiatric disorders in humans (Phelps, 2004; Richardson et al., 2004) and in animal models (Ghosh et al., 2013; Santos et al., 2013; Zhang et al., 2014). "
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    ABSTRACT: The dynamic interactions between hippocampus and amygdala are critical for emotional memory. Theta synchrony between these structures occurs during fear memory retrieval and may facilitate synaptic plasticity, but the cellular mechanisms are unknown. We report that interneurons of the mouse basal amygdala are activated during theta network activity or optogenetic stimulation of ventral CA1 pyramidal cell axons, whereas principal neurons are inhibited. Interneurons provide feedforward inhibition that transiently hyperpolarizes principal neurons. However, synaptic inhibition attenuates during theta frequency stimulation of ventral CA1 fibers, and this broadens excitatory postsynaptic potentials. These effects are mediated by GABAB receptors and change in the Cl(-) driving force. Pairing theta frequency stimulation of ventral CA1 fibers with coincident stimuli of the lateral amygdala induces long-term potentiation of lateral-basal amygdala excitatory synapses. Hence, feedforward inhibition, known to enforce temporal fidelity of excitatory inputs, dominates hippocampus-amygdala interactions to gate heterosynaptic plasticity. VIDEO ABSTRACT.
    Neuron 09/2015; 87(6):1290-1303. DOI:10.1016/j.neuron.2015.08.024 · 15.05 Impact Factor
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    • "The systemic effects of SB 242084 may help elucidate some of the anatomical loci of fear discrimination learning. The basolateral amygdala, a critical site of neuroplasticity mediating the acquisition and recall of conditioned fear in rodents (Maren and Quirk, 2004) and humans (Milad et al., 2006; Rauch, et al., 2006b), is the locus of 5-HT action for stressor-induced anxiety (Christianson et al., 2010), stressor enhanced fear (Baratta et al., 2015) and selective serotonin reuptake inhibitor induced anxiety (Vicente and Zangrossi, 2012). Regarding reversal learning, the orbital frontal cortex, which is critical for task response switching as predicted values change (for reviews see Schoenbaum et al., 2011; McDannald et al., 2014) is also modulated by the 5-HT 2C receptor, with SB 242084 improving reversal learning when applied by local microinjection (Boulougouris and Robbins, 2010). "
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    ABSTRACT: Ethical statement: John P. Christianson and Allison R. Foilb, the authors, verify that animal research was carried out in accordance with the National Institute of Health Guide for the Care and Use of Laboratory Animals (NIH Publications No. 80-23) and all procedures involving animals were reviewed and approved by the Boston College Animal Care and Use Committee. All efforts were made to limit the number of animals used and their suffering.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 09/2015; DOI:10.1016/j.pnpbp.2015.08.017 · 3.69 Impact Factor
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    • "The amygdala is the core brain structure in rodent and human fear expression, acquisition and extinction (Herry et al., 2008; Hitchcock and Davis, 1986; Maren and Quirk, 2004; Sierra-Mercado et al., 2011) and has an important role in fear-related disorders. Structural magnetic resonance imaging (MRI) studies have consistently reported a reduction in amygdala volume in PD patients (Asami et al., 2009; Hayano et al., 2009; Massana et al., 2003b; Uchida et al., 2003). "
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    ABSTRACT: Fear is an ancestral emotion, an intrinsic defensive response present in every organism. Although fear is an evolutionarily advantageous emotion, under certain pathologies such as panic disorder it might become exaggerated and non-adaptive. Clinical and preclinical work pinpoints that changes in cognitive processes, such as perception and interpretation of environmental stimuli that rely on brain regions responsible for high-level function, are essential for the development of fear-related disorders. This review focuses on the involvement of cognitive function to fear circuitry disorders. Moreover, we address how animal models are contributing to understand the involvement of human candidate genes to pathological fear and helping achieve progress in this field. Multidisciplinary approaches that integrate human genetic findings with state of the art genetic mouse models will allow to elucidate the mechanisms underlying pathology and to develop new strategies for therapeutic targeting. Copyright © 2015. Published by Elsevier B.V.
    European journal of pharmacology 03/2015; 759. DOI:10.1016/j.ejphar.2015.03.039 · 2.53 Impact Factor
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