000272575 001__ 272575
000272575 005__ 20241013000018.0
000272575 0247_ $$2doi$$a10.1101/2024.09.29.612271
000272575 0247_ $$2altmetric$$aaltmetric:168772822
000272575 037__ $$aDZNE-2024-01196
000272575 082__ $$a570
000272575 1001_ $$0P:(DE-2719)9001992$$aFavila, Natalia$$b0$$eFirst author
000272575 245__ $$aHeterogeneous plasticity of amygdala interneurons in associative learning and extinction
000272575 260__ $$aCold Spring Harbor$$bCold Spring Harbor Laboratory, NY$$c2024
000272575 3367_ $$0PUB:(DE-HGF)25$$2PUB:(DE-HGF)$$aPreprint$$bpreprint$$mpreprint$$s1728571361_9468
000272575 3367_ $$2ORCID$$aWORKING_PAPER
000272575 3367_ $$028$$2EndNote$$aElectronic Article
000272575 3367_ $$2DRIVER$$apreprint
000272575 3367_ $$2BibTeX$$aARTICLE
000272575 3367_ $$2DataCite$$aOutput Types/Working Paper
000272575 520__ $$aNeural circuits undergo experience-dependent plasticity to form long-lasting memories. Excitatory projection neurons are considered to be the primary neuronal substrate for memory acquisition and storage. However, inhibitory interneurons control the activity of projection neurons in a in a spatially and temporally precise manner, yet their contribution to memory acquisition, storage and expression remains poorly understood. Here, we employ a miniature microscope imaging approach to monitor the activity of large amygdala interneuron populations in freely moving mice during fear learning and extinction at the single cell level. We find that amygdala interneurons display mixed-selectivity and show complex plastic responses at both the ensemble and single neuron level across the acquisition, expression and extinction of aversive memories. In contrast to bidirectional single cell plasticity across distinct fear states, learning-induced changes at the population level occur transiently during conditioning and do not consolidate across days. Examining molecular interneuron subpopulations revealed that disinhibitory vasoactive intestinal peptide (VIP) expressing cells are predominantly activated by high fear states. In contrast, somatostatin (SST) interneurons display a preference for safety cues and thereby suppress excitatory neuron responsiveness. However, responses of individual neurons within the SST and VIP populations are non-uniform, indicating the presence of functional subtypes within classical molecularly-defined interneuron populations. Taken together, we identify complex neuronal plasticity within amygdala interneuron ensembles that goes beyond a passive processing function, suggesting a critical role of inhibitory microcircuit elements for memory selectivity and stability.
000272575 536__ $$0G:(DE-HGF)POF4-351$$a351 - Brain Function (POF4-351)$$cPOF4-351$$fPOF IV$$x0
000272575 588__ $$aDataset connected to CrossRef
000272575 7001_ $$0P:(DE-2719)9001352$$aCapece-Marsico, Jessica$$b1$$udzne
000272575 7001_ $$0P:(DE-2719)9002151$$aEscribano, Benjamin$$b2$$udzne
000272575 7001_ $$0P:(DE-2719)9001811$$aPacheco, Catarina$$b3$$udzne
000272575 7001_ $$00000-0002-4153-3888$$aBitterman, Yael$$b4
000272575 7001_ $$0P:(DE-2719)9001219$$aGründemann, Jan$$b5
000272575 7001_ $$00000-0002-1859-4252$$aLüthi, Andreas$$b6
000272575 7001_ $$0P:(DE-2719)9001056$$aKrabbe, Sabine$$b7$$eLast author
000272575 773__ $$0PERI:(DE-600)2766415-6$$a10.1101/2024.09.29.612271$$tbioRxiv beta$$y2024
000272575 8564_ $$uhttps://pub.dzne.de/record/272575/files/DZNE-2024-01196_Preprint.pdf$$yOpenAccess
000272575 8564_ $$uhttps://pub.dzne.de/record/272575/files/DZNE-2024-01196_Preprint.pdf?subformat=pdfa$$xpdfa$$yOpenAccess
000272575 909CO $$ooai:pub.dzne.de:272575$$pdnbdelivery$$pdriver$$pVDB$$popen_access$$popenaire
000272575 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9001992$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b0$$kDZNE
000272575 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9001352$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b1$$kDZNE
000272575 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9002151$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b2$$kDZNE
000272575 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9001811$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b3$$kDZNE
000272575 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9001219$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b5$$kDZNE
000272575 9101_ $$0I:(DE-588)1065079516$$6P:(DE-2719)9001056$$aDeutsches Zentrum für Neurodegenerative Erkrankungen$$b7$$kDZNE
000272575 9131_ $$0G:(DE-HGF)POF4-351$$1G:(DE-HGF)POF4-350$$2G:(DE-HGF)POF4-300$$3G:(DE-HGF)POF4$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lNeurodegenerative Diseases$$vBrain Function$$x0
000272575 9141_ $$y2024
000272575 915__ $$0StatID:(DE-HGF)0510$$2StatID$$aOpenAccess
000272575 915__ $$0LIC:(DE-HGF)CCBY4$$2HGFVOC$$aCreative Commons Attribution CC BY 4.0
000272575 9201_ $$0I:(DE-2719)5000059$$kAG Krabbe$$lFunctional Diversity of Neural Circuits$$x0
000272575 9201_ $$0I:(DE-2719)5000069$$kAG Gründemann$$lNeural Circuit Computations$$x1
000272575 980__ $$apreprint
000272575 980__ $$aVDB
000272575 980__ $$aUNRESTRICTED
000272575 980__ $$aI:(DE-2719)5000059
000272575 980__ $$aI:(DE-2719)5000069
000272575 9801_ $$aFullTexts