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000141303 0247_ $$2ISSN$$a1740-634X
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000141303 1001_ $$aLange, Maren D$$b0
000141303 245__ $$aGlutamic acid decarboxylase 65: a link between GABAergic synaptic plasticity in the lateral amygdala and conditioned fear generalization.
000141303 260__ $$aBasingstoke$$bNature Publishing Group71819$$c2014
000141303 264_1 $$2Crossref$$3online$$bSpringer Science and Business Media LLC$$c2014-03-25
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000141303 520__ $$aAn imbalance of the gamma-aminobutyric acid (GABA) system is considered a major neurobiological pathomechanism of anxiety, and the amygdala is a key brain region involved. Reduced GABA levels have been found in anxiety patients, and genetic variations of glutamic acid decarboxylase (GAD), the rate-limiting enzyme of GABA synthesis, have been associated with anxiety phenotypes in both humans and mice. These findings prompted us to hypothesize that a deficiency of GAD65, the GAD isoform controlling the availability of GABA as a transmitter, affects synaptic transmission and plasticity in the lateral amygdala (LA), and thereby interferes with fear responsiveness. Results indicate that genetically determined GAD65 deficiency in mice is associated with (1) increased synaptic length and release at GABAergic connections, (2) impaired efficacy of GABAergic synaptic transmission and plasticity, and (3) reduced spillover of GABA to presynaptic GABAB receptors, resulting in a loss of the associative nature of long-term synaptic plasticity at cortical inputs to LA principal neurons. (4) In addition, training with high shock intensities in wild-type mice mimicked the phenotype of GAD65 deficiency at both the behavioral and synaptic level, indicated by generalization of conditioned fear and a loss of the associative nature of synaptic plasticity in the LA. In conclusion, GAD65 is required for efficient GABAergic synaptic transmission and plasticity, and for maintaining extracellular GABA at a level needed for associative plasticity at cortical inputs in the LA, which, if disturbed, results in an impairment of the cue specificity of conditioned fear responses typifying anxiety disorders.
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000141303 650_7 $$2NLM Chemicals$$aReceptors, GABA-B
000141303 650_7 $$03KX376GY7L$$2NLM Chemicals$$aGlutamic Acid
000141303 650_7 $$056-12-2$$2NLM Chemicals$$agamma-Aminobutyric Acid
000141303 650_7 $$0EC 4.1.1.15$$2NLM Chemicals$$aGlutamate Decarboxylase
000141303 650_7 $$0EC 4.1.1.15$$2NLM Chemicals$$aglutamate decarboxylase 2
000141303 650_2 $$2MeSH$$aAmygdala: cytology
000141303 650_2 $$2MeSH$$aAmygdala: enzymology
000141303 650_2 $$2MeSH$$aAnimals
000141303 650_2 $$2MeSH$$aAssociation Learning: physiology
000141303 650_2 $$2MeSH$$aConditioning, Psychological: physiology
000141303 650_2 $$2MeSH$$aElectroshock
000141303 650_2 $$2MeSH$$aExtracellular Space: metabolism
000141303 650_2 $$2MeSH$$aFear: physiology
000141303 650_2 $$2MeSH$$aGeneralization, Psychological: physiology
000141303 650_2 $$2MeSH$$aGlutamate Decarboxylase: genetics
000141303 650_2 $$2MeSH$$aGlutamate Decarboxylase: metabolism
000141303 650_2 $$2MeSH$$aGlutamic Acid: metabolism
000141303 650_2 $$2MeSH$$aInterneurons: cytology
000141303 650_2 $$2MeSH$$aInterneurons: physiology
000141303 650_2 $$2MeSH$$aLong-Term Potentiation: physiology
000141303 650_2 $$2MeSH$$aMale
000141303 650_2 $$2MeSH$$aMice, Inbred C57BL
000141303 650_2 $$2MeSH$$aMice, Knockout
000141303 650_2 $$2MeSH$$aNeurons: cytology
000141303 650_2 $$2MeSH$$aNeurons: physiology
000141303 650_2 $$2MeSH$$aReceptors, GABA-B: metabolism
000141303 650_2 $$2MeSH$$aSynaptic Transmission: physiology
000141303 650_2 $$2MeSH$$agamma-Aminobutyric Acid: metabolism
000141303 7001_ $$aJüngling, Kay$$b1
000141303 7001_ $$aPaulukat, Linda$$b2
000141303 7001_ $$aVieler, Marc$$b3
000141303 7001_ $$aGaburro, Stefano$$b4
000141303 7001_ $$0P:(DE-2719)2810715$$aSosulina, Liudmila$$b5$$udzne
000141303 7001_ $$aBlaesse, Peter$$b6
000141303 7001_ $$aSreepathi, Hari K$$b7
000141303 7001_ $$aFerraguti, Francesco$$b8
000141303 7001_ $$0P:(DE-HGF)0$$aPape, Hans-Christian$$b9$$eCorresponding author
000141303 77318 $$2Crossref$$3journal-article$$a10.1038/npp.2014.72$$bSpringer Science and Business Media LLC$$d2014-03-25$$n9$$p2211-2220$$tNeuropsychopharmacology$$v39$$x0893-133X$$y2014
000141303 773__ $$0PERI:(DE-600)2008300-2$$a10.1038/npp.2014.72$$gVol. 39, no. 9, p. 2211 - 2220$$n9$$p2211-2220$$q39:9<2211 - 2220$$tNeuropsychopharmacology$$v39$$x0893-133X$$y2014
000141303 8567_ $$2Pubmed Central$$uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4104340
000141303 8564_ $$uhttps://pub.dzne.de/record/141303/files/DZNE-2020-07625_Restricted.pdf
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000141303 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)2810715$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b5$$kDZNE
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