JankovicV1, Pmc, Checkpoint, bibRecord, 000187

Increased c-fos expression in the central nucleus of the amygdala and enhancement of cued fear memory in Dyt1 ΔGAG knock-in mice

Identifieur interne : 000187 ( Pmc/Checkpoint ); précédent : 000186; suivant : 000188

Increased c-fos expression in the central nucleus of the amygdala and enhancement of cued fear memory in Dyt1 ΔGAG knock-in mice

Auteurs : Fumiaki Yokoi [États-Unis] ; Mai Dang [États-Unis] ; Courtney Miller [États-Unis] ; Andrea Marshall [États-Unis] ; Susan Campbell [États-Unis] ; J Sweatt [États-Unis] ; Yuqing Li [États-Unis]

Source :

Neuroscience research [ 0168-0102 ] ; 2009.

RBID : PMC:2757526

Abstract

DYT1 dystonia is caused by a trinucleotide deletion of GAG (ΔGAG) in DYT1, which codes for torsinA. A previous epidemiologic study suggested an association of DYT1 ΔGAG mutation with early-onset recurrent major depression. However, another study reported no significant association with depression, but instead showed an association with anxiety and dystonia. In this study, we analyzed these related behaviors in Dyt1 ΔGAG heterozygous knock-in mice. The knock-in mice showed a subtle anxiety-like behavior but did not show depression-like behaviors. The mutant mice also displayed normal sensorimotor gating function in a prepulse inhibition test. While normal hippocampus-dependent contextual fear memory and hippocampal CA1 long-term potentiation (LTP) were observed, the knock-in mice exhibited an enhancement in the formation of cued fear memories. Anatomical analysis indicated that the number of c-fos positive cells was significantly increased while the size of the central nucleus of the amygdala (CE) was significantly reduced in the knock-in mice. These results suggest that the Dyt1 ΔGAG mutation increased the activity of the CE and enhanced the acquisition of the cued fear memory.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757526

DOI: 10.1016/j.neures.2009.07.004
PubMed: 19619587
PubMed Central: 2757526

Affiliations:

États-Unis

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<front><div type="abstract" xml:lang="en"><p id="P1">DYT1 dystonia is caused by a trinucleotide deletion of GAG (ΔGAG) in <italic>DYT1</italic>
, which codes for torsinA. A previous epidemiologic study suggested an association of <italic>DYT1</italic>
 ΔGAG mutation with early-onset recurrent major depression. However, another study reported no significant association with depression, but instead showed an association with anxiety and dystonia. In this study, we analyzed these related behaviors in <italic>Dyt1</italic>
 ΔGAG heterozygous knock-in mice. The knock-in mice showed a subtle anxiety-like behavior but did not show depression-like behaviors. The mutant mice also displayed normal sensorimotor gating function in a prepulse inhibition test. While normal hippocampus-dependent contextual fear memory and hippocampal CA1 long-term potentiation (LTP) were observed, the knock-in mice exhibited an enhancement in the formation of cued fear memories. Anatomical analysis indicated that the number of c-fos positive cells was significantly increased while the size of the central nucleus of the amygdala (CE) was significantly reduced in the knock-in mice. These results suggest that the <italic>Dyt1</italic>
 ΔGAG mutation increased the activity of the CE and enhanced the acquisition of the cued fear memory.</p>
</div>
</front>
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<title-group><article-title>Increased c-fos expression in the central nucleus of the amygdala and enhancement of cued fear memory in <italic>Dyt1</italic>
 ΔGAG knock-in mice</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Yokoi</surname>
<given-names>Fumiaki</given-names>
</name>
<xref rid="A1" ref-type="aff">1</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Dang</surname>
<given-names>Mai T.</given-names>
</name>
<xref rid="A2" ref-type="aff">2</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Miller</surname>
<given-names>Courtney A.</given-names>
</name>
<xref rid="A4" ref-type="aff">4</xref>
<xref rid="A5" ref-type="aff">5</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Marshall</surname>
<given-names>Andrea G.</given-names>
</name>
<xref rid="A3" ref-type="aff">3</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Campbell</surname>
<given-names>Susan L.</given-names>
</name>
<xref rid="A4" ref-type="aff">4</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Sweatt</surname>
<given-names>J. David</given-names>
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<xref rid="A4" ref-type="aff">4</xref>
<xref rid="A5" ref-type="aff">5</xref>
</contrib>
<contrib contrib-type="author"><name><surname>Li</surname>
<given-names>Yuqing</given-names>
</name>
<xref rid="A1" ref-type="aff">1</xref>
<xref rid="A3" ref-type="aff">3</xref>
<xref rid="A4" ref-type="aff">4</xref>
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<aff id="A1"><label>1</label>
Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA</aff>
<aff id="A2"><label>2</label>
Medical Scholars Program, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA</aff>
<aff id="A3"><label>3</label>
Neuroscience Program, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA</aff>
<aff id="A4"><label>4</label>
Department of Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA</aff>
<aff id="A5"><label>5</label>
Evelyn F. McKnight Brain Institute, School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA</aff>
<author-notes><corresp id="FN1"><label>*</label>
Correspondence author at: CIRC 560, 1530 3<sup>rd</sup>
 Avenue South, Birmingham, Alabama 35294-0017, USA. Tel.:+1-205-996-6299, Fax: +1-205-996-7200. E-mail address: <email>yli@uab.edu</email>
 (Y. Li)</corresp>
<fn id="FN2"><p>Receiving Editor: Prof. Nobumasa Kato, M.D. & Ph.D., Department of Psychiatry, Showa University School of Medicine</p>
</fn>
</author-notes>
<pub-date pub-type="nihms-submitted"><day>24</day>
<month>7</month>
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<year>2010</year>
</pub-date>
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<issue>3</issue>
<fpage>228</fpage>
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<abstract><p id="P1">DYT1 dystonia is caused by a trinucleotide deletion of GAG (ΔGAG) in <italic>DYT1</italic>
, which codes for torsinA. A previous epidemiologic study suggested an association of <italic>DYT1</italic>
 ΔGAG mutation with early-onset recurrent major depression. However, another study reported no significant association with depression, but instead showed an association with anxiety and dystonia. In this study, we analyzed these related behaviors in <italic>Dyt1</italic>
 ΔGAG heterozygous knock-in mice. The knock-in mice showed a subtle anxiety-like behavior but did not show depression-like behaviors. The mutant mice also displayed normal sensorimotor gating function in a prepulse inhibition test. While normal hippocampus-dependent contextual fear memory and hippocampal CA1 long-term potentiation (LTP) were observed, the knock-in mice exhibited an enhancement in the formation of cued fear memories. Anatomical analysis indicated that the number of c-fos positive cells was significantly increased while the size of the central nucleus of the amygdala (CE) was significantly reduced in the knock-in mice. These results suggest that the <italic>Dyt1</italic>
 ΔGAG mutation increased the activity of the CE and enhanced the acquisition of the cued fear memory.</p>
</abstract>
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<name sortKey="Li, Yuqing" sort="Li, Yuqing" uniqKey="Li Y" first="Yuqing" last="Li">Yuqing Li</name>
<name sortKey="Li, Yuqing" sort="Li, Yuqing" uniqKey="Li Y" first="Yuqing" last="Li">Yuqing Li</name>
<name sortKey="Li, Yuqing" sort="Li, Yuqing" uniqKey="Li Y" first="Yuqing" last="Li">Yuqing Li</name>
<name sortKey="Marshall, Andrea G" sort="Marshall, Andrea G" uniqKey="Marshall A" first="Andrea" last="Marshall">Andrea Marshall</name>
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	Serveur d'exploration autour de Joseph Jankovic
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Serveur d'exploration autour de Joseph Jankovic

Increased c-fos expression in the central nucleus of the amygdala and enhancement of cued fear memory in Dyt1 ΔGAG knock-in mice

Increased c-fos expression in the central nucleus of the amygdala and enhancement of cued fear memory in Dyt1 ΔGAG knock-in mice

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