Article

Neuronal signalling of fear memory.

Department of Psychology and Neuroscience Program, University of Michigan, Ann Arbor, Michigan 48109, USA.
Nature reviews Neuroscience (Impact Factor: 31.38). 12/2004; 5(11):844-52. DOI: 10.1038/nrn1535
Source: PubMed

ABSTRACT 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.

Download full-text

Full-text

Available from: Stephen Maren, Jun 29, 2015
0 Followers
 · 
130 Views
  • Source
    [Show abstract] [Hide abstract]
    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 · 2.68 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Serotonin facilitates fear learning in animals. We therefore predicted that individual differences in the capacity to regulate serotonergic transmission in the human neural fear circuit would be inversely related to fear conditioning. The capacity to regulate serotonergic transmission was indexed by serotonin transporter availability measured with [(11)C]-DASB positron emission tomography. Results indicate that lower serotonin transporter availability in the amygdala, insula and dorsal anterior cingulate cortex predicts enhanced conditioned autonomic fear responses. Our finding support serotonergic modulation of fear conditioning in humans and may aid in understanding susceptibility for developing anxiety conditions such as post-traumatic stress disorder. Copyright © 2014. Published by Elsevier B.V.
    International journal of psychophysiology: official journal of the International Organization of Psychophysiology 12/2014; DOI:10.1016/j.ijpsycho.2014.12.002 · 2.65 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: There is conflicting evidence regarding whether calcium-permeable receptors are removed during group I mGluR-mediated synaptic depression. In support of this hypothesis, AMPAR rectification, a correlative index of the synaptic expression of GluA2-lacking calcium-permeable AMPARs (CP-AMPARs), is known to decrease after the induction of several types of group I mGluR-mediated long-term depression (LTD), suggesting that a significant proportion of synaptic CP-AMPARs is removed during synaptic depression. We have previously demonstrated that fear conditioning-induced synaptic potentiation in the lateral amygdala is reversed by group 1 mGluR-mediated depotentiation. Here, we examined whether CP-AMPARs are removed by mGluR1-mediated depotentiation of fear conditioning-induced synaptic potentiation. The synaptic expression of CP-AMPARs was negligible before, increased significantly 12 h after, and returned to baseline 48 h after fear conditioning, as evidenced by the changes in the sensitivity of lateral amygdala synaptic responses to NASPM. Importantly, the sensitivity to NASPM was not altered after induction of depotentiation. Our findings, together with previous results, suggest that the removal of CP-AMPARs is not required for the depotentiation of fear conditioning-induced synaptic potentiation at lateral amygdala synapses.
    Frontiers in Behavioral Neuroscience 08/2014; 8:269. DOI:10.3389/fnbeh.2014.00269 · 4.16 Impact Factor