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      Immediate Early Genes, Memory and Psychiatric Disorders: Focus on c-Fos, Egr1 and Arc

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          Abstract

          Many psychiatric disorders, despite their specific characteristics, share deficits in the cognitive domain including executive functions, emotional control and memory. However, memory deficits have been in many cases undervalued compared with other characteristics. The expression of Immediate Early Genes (IEGs) such as, c-fos, Egr1 and arc are selectively and promptly upregulated in learning and memory among neuronal subpopulations in regions associated with these processes. Changes in expression in these genes have been observed in recognition, working and fear related memories across the brain. Despite the enormous amount of data supporting changes in their expression during learning and memory and the importance of those cognitive processes in psychiatric conditions, there are very few studies analyzing the direct implication of the IEGs in mental illnesses. In this review, we discuss the role of some of the most relevant IEGs in relation with memory processes affected in psychiatric conditions.

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          Most cited references253

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          Animal models of neuropsychiatric disorders.

          Modeling of human neuropsychiatric disorders in animals is extremely challenging given the subjective nature of many symptoms, the lack of biomarkers and objective diagnostic tests, and the early state of the relevant neurobiology and genetics. Nonetheless, progress in understanding pathophysiology and in treatment development would benefit greatly from improved animal models. Here we review the current state of animal models of mental illness, with a focus on schizophrenia, depression and bipolar disorder. We argue for areas of focus that might increase the likelihood of creating more useful models, at least for some disorders, and for explicit guidelines when animal models are reported.
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            Optogenetic stimulation of a hippocampal engram activates fear memory recall

            A specific memory is thought to be encoded by a sparse population of neurons 1,2 . These neurons can be tagged during learning for subsequent identification 3 and manipulation 4,5,6 . Moreover, their ablation or inactivation results in reduced memory expression, suggesting their necessity in mnemonic processes. However, a critical question of sufficiency remains: can one elicit the behavioral output of a specific memory by directly activating a population of neurons that was active during learning? Here we show that optogenetic reactivation of hippocampal neurons activated during fear conditioning is sufficient to induce freezing behavior. We labeled a population of hippocampal dentate gyrus neurons activated during fear learning with channelrhodopsin-2 (ChR2) 7,8 and later optically reactivated these neurons in a different context. The mice showed increased freezing only upon light stimulation, indicating light-induced fear memory recall. This freezing was not detected in non-fear conditioned mice expressing ChR2 in a similar proportion of cells, nor in fear conditioned mice with cells labeled by EYFP instead of ChR2. Finally, activation of cells labeled in a context not associated with fear did not evoke freezing in mice that were previously fear conditioned in a different context, suggesting that light-induced fear memory recall is context-specific. Together, our findings indicate that activating a sparse but specific ensemble of hippocampal neurons that contribute to a memory engram is sufficient for the recall of that memory. Moreover, our experimental approach offers a general method of mapping cellular populations bearing memory engrams.
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              Neural mechanisms of extinction learning and retrieval.

              Emotional learning is necessary for individuals to survive and prosper. Once acquired, however, emotional associations are not always expressed. Indeed, the regulation of emotional expression under varying environmental conditions is essential for mental health. The simplest form of emotional regulation is extinction, in which conditioned responding to a stimulus decreases when the reinforcer is omitted. Two decades of research on the neural mechanisms of fear conditioning have laid the groundwork for understanding extinction. In this review, we summarize recent work on the neural mechanisms of extinction learning. Like other forms of learning, extinction occurs in three phases: acquisition, consolidation, and retrieval, each of which depends on specific structures (amygdala, prefrontal cortex, hippocampus) and molecular mechanisms (receptors and signaling pathways). Pharmacological methods to facilitate consolidation and retrieval of extinction, for both aversive and appetitive conditioning, are setting the stage for novel treatments for anxiety disorders and addictions.
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                Author and article information

                Contributors
                Journal
                Front Behav Neurosci
                Front Behav Neurosci
                Front. Behav. Neurosci.
                Frontiers in Behavioral Neuroscience
                Frontiers Media S.A.
                1662-5153
                25 April 2018
                2018
                : 12
                Affiliations
                [1] 1Instituto de Fisiología y Biofísica Bernardo Houssay, Departamento de Fisiología, Facultad de Medicina, Universidad de Buenos Aires (UBA) , Buenos Aires, Argentina
                [2] 2Instituto de Biología Celular y Neurociencias (IBCN) Dr. Eduardo de Robertis, Facultad de Medicina, CONICET, Universidad de Buenos Aires (UBA) , Buenos Aires, Argentina
                [3] 3Departamento de Fisiología, Facultad de Medicina, Universidad de Buenos (UBA) , Buenos Aires, Argentina
                Author notes

                Edited by: Amelia Gallitano, University of Arizona, United States

                Reviewed by: Francesco Papaleo, Fondazione Istituto Italiano di Technologia, Italy; Andrea De Bartolomeis, University of Naples Federico II, Italy

                These authors have contributed equally to this work.

                Present address: Francisco T. Gallo, Instituto de Neurociencia Cognitiva y Translacional, Universidad Favaloro, INECO, CONICET, Buenos Aires, Argentina; Juan F. Morici, Instituto de Neurociencia Cognitiva y Translacional, Universidad Favaloro, INECO, CONICET, Buenos Aires, Argentina; Noelia V. Weisstaub, Instituto de Neurociencia Cognitiva y Translacional, Universidad Favaloro, INECO, CONICET, Buenos Aires, Argentina

                Article
                10.3389/fnbeh.2018.00079
                5932360
                29755331
                f232db25-734a-4fe0-98e4-c2266cefb2bf
                Copyright © 2018 Gallo, Katche, Morici, Medina and Weisstaub.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 287, Pages: 16, Words: 15989
                Funding
                Funded by: Agencia Nacional de Promoción Científica y Tecnológica 10.13039/501100003074
                Award ID: PICT2015-2344, PICT2015-1552, PICT2013-0335
                Categories
                Neuroscience
                Review

                Neurosciences
                egr1,c-fos,arc,fear memory,episodic memory,rodents,psychiatric disorders
                Neurosciences
                egr1, c-fos, arc, fear memory, episodic memory, rodents, psychiatric disorders

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