{"id":17529,"date":"2022-09-19T15:28:03","date_gmt":"2022-09-19T13:28:03","guid":{"rendered":"https:\/\/www.neurosciences.asso.fr\/2022\/09\/formation-de-la-memoire-sociale-plasticites-en-cascade-dans-lhippocampe\/"},"modified":"2022-09-19T15:30:26","modified_gmt":"2022-09-19T13:30:26","slug":"formation-de-la-memoire-sociale-plasticites-en-cascade-dans-lhippocampe","status":"publish","type":"post","link":"https:\/\/www.neurosciences.asso.fr\/en\/2022\/09\/formation-de-la-memoire-sociale-plasticites-en-cascade-dans-lhippocampe\/","title":{"rendered":"FORMATION DE LA MEMOIRE SOCIALE : PLASTICITES EN CASCADE DANS L&#8217;HIPPOCAMPE"},"content":{"rendered":"<p>La cognition sociale est une fonction importante pour de nombreuses esp\u00e8ces qui est alt\u00e9r\u00e9e lors de maladies psychiatriques et neurod\u00e9g\u00e9n\u00e9ratives. Bien que l\u2019hippocampe et en particulier la r\u00e9gion CA2 soient connus pour jouer un r\u00f4le cl\u00e9 dans la formation de m\u00e9moire sociale, les m\u00e9canismes cellulaires impliqu\u00e9s ne sont pas connus.<\/p>\n<p>Dans une \u00e9tude r\u00e9cente r\u00e9alis\u00e9e sur des souris, nous d\u00e9crivons comment deux plasticit\u00e9s synaptiques de la transmission inhibitrice dans CA2 pourraient \u00eatre d\u00e9clench\u00e9es afin de coder l\u2019identit\u00e9 d\u2019une nouvelle souris et d\u2019en former une m\u00e9moire \u00e0 long-terme.<\/p>\n<p>Plus pr\u00e9cis\u00e9ment, nous montrons comment l\u2019exposition d\u2019une souris \u00e0 un nouvel individu induit tout d\u2019abord une d\u00e9pression \u00e0 long-terme de la transmission inhibitrice des interneurones exprimant la parvalbumine par l\u2019interm\u00e9diaire de r\u00e9cepteurs delta-opio\u00efdes. La diminution de la transmission inhibitrice permet ensuite aux neurones principaux de CA2 de g\u00e9n\u00e9rer des potentiels d\u2019actions et d\u2019induire une deuxi\u00e8me d\u00e9pression \u00e0 long-terme de la transmission inhibitrice par l\u2019activation des r\u00e9cepteurs cannabinoides de type I (CB1) sur les interneurones exprimant la chol\u00e9cystokinine. Le blocage des r\u00e9cepteurs CB1 dans la r\u00e9gion CA2 emp\u00eache compl\u00e8tement la formation de m\u00e9moire sociale. Par ailleurs, la plasticit\u00e9 d\u00e9pendante des r\u00e9cepteurs CB1 est fortement diminu\u00e9e sur un mod\u00e8le murin de schizophr\u00e9nie, qui a aussi un fort d\u00e9ficit de m\u00e9moire sociale. Enfin, une manipulation pharmacologique de l\u2019excitabilit\u00e9 des neurones principaux de CA2, qui \u00e9tait connue pour am\u00e9liorer la m\u00e9moire sociale sur ces souris, restaure aussi la plasticit\u00e9 induite par les r\u00e9cepteurs CB1.<\/p>\n<p>Ces r\u00e9sultats montrent l\u2019importance de l\u2019interaction entre deux plasticit\u00e9s inhibitrices dans la formation de m\u00e9moire sociale et offrent de nouvelles perspectives de traitement dans des pathologies avec alt\u00e9ration de la cognition sociale.<\/p>\n<p>&nbsp;<\/p>\n<p><em><strong>L\u00e9gende de la figure:<\/strong><\/em><\/p>\n<p>En condition basale, la transmission synaptique entre les neurones pyramidaux CA3 et CA2 est domin\u00e9e par une importante inhibition de type &#8216;feed-forward&#8217; emp\u00eachant les neurones pyramidaux de CA2 de d\u00e9clencher des potentiels d&#8217;action (PA). Lorsqu&#8217;une souris est expos\u00e9e \u00e0 une nouvelle souris, une d\u00e9pression \u00e0 long terme de la transmission inhibitrice des interneurones exprimant la parvalbumine (PV-IN) est induite par l&#8217;activation des r\u00e9cepteurs Delta-opio\u00efdes (DOR-iLTD). Cette d\u00e9sinhibition permet aux PN de CA2 de g\u00e9n\u00e9rer des PA en r\u00e9ponse \u00e0 l&#8217;activation des entr\u00e9es de CA3. Apr\u00e8s une exposition ult\u00e9rieure \u00e0 la nouvelle souris, les PN qui d\u00e9clenchent suffisamment de PA expriment une deuxi\u00e8me iLTD m\u00e9di\u00e9e par l&#8217;activation des r\u00e9cepteurs cannabino\u00efdes de type I (CB1R-iLTD), ce qui augmente encore le d\u00e9clenchement de PA dans ces PN.<\/p>\n<p>&nbsp;<\/p>\n<p><em><strong>R\u00e9ference :<\/strong><\/em><\/p>\n<p>Sequential inhibitory plasticities in hippocampal area CA2 and social memory formation.<\/p>\n<p>Loisy M, Bouisset G, Lopez S, Muller M, Spitsyn A, Duval J, Piskorowski RA, Verret L, Chevaleyre V. Neuron. 2022; 110(17):2854-66 doi: 10.1016\/j.neuron.2022.06.013.<\/p>\n<p>&nbsp;<\/p>\n<p><em><strong>Contacts :<\/strong><\/em><\/p>\n<p>Vivien Chevaleyre \/ Rebecca Piskorowski: Universit\u00e9 Paris Cit\u00e9, INSERM U1266, Institute of Psychiatry and Neuroscience of Paris, 75014 Paris, France<\/p>\n<p>Laure Verret: Research Center on Animal Cognition, Center for Integrative Biology, Toulouse University, CNRS, UPS, 31062 Toulouse, France<\/p>\n<p>&nbsp;<\/p>\n<p><strong><em>English summary:<\/em><\/strong><\/p>\n<p><em>Social cognition is a key function for numerous species and is altered during several psychiatric and neurodegenerative diseases. While the hippocampus and in particular area CA2 are known to play a critical role in social memory formation, the underlying cellular mechanisms are not known.<\/em><\/p>\n<p><em>In a recent study performed in mice, we describe how two synaptic plasticities of inhibitory transmission could be induced during the coding of a novel mouse and the formation of a lasting memory.<\/em><\/p>\n<p><em>More precisely, we show how exposure to a novel mouse induces a long-term depression of inhibitory transmission form parvalbumin-expressing interneuron via activation of delta-opioid receptors. The resulting dis-inhibition allows principal cells in CA2 to fire action potentials and to evoke a second long-term depression of inhibition from cholecystokinin-expressing interneurons through activation of cannabinoid type I receptors (CB1). Blockade of CB1 receptors in area CA2 completely prevents social memory formation. Furthermore, CB1-mediated plasticity is strongly reduced in a mouse model of schizophrenia with impaired social memory. Finally, pharmacological manipulation known to improve social memory in these mice also restores CB1-mediated plasticity.<\/em><\/p>\n<p><em>These results highlight how interaction between two inhibitory plasticities plays an important role in social memory formation and reveal new therapeutic targets for pathologies with social cognition impairments.<\/em><\/p>\n<p>&nbsp;<\/p>\n<p><em><strong>Figure Legend :<\/strong><\/em><\/p>\n<p>In basal condition, synaptic drive between CA3 and CA2 pyramidal neurons (PN) is dominated by a large feed-forward inhibition preventing CA2 PNs to fire action potentials (AP). When a mouse is exposed to a novel mouse, a long-term depression of inhibitory transmission from parvalbumin-expressing interneurons (PV-IN) is induced by activation of Delta-opioid receptors (DOR-iLTD). This disinhibition allows CA2 PNs to fire APs in response to CA3 inputs activation. Following subsequent exposure to the novel mouse, PNs that fire enough APs express a second iLTD mediated by activation of cannabinoid type I receptors (CB1R-iLTD), hence further increasing AP firing in these PNs.<\/p>\n<p>&nbsp;<\/p>\n","protected":false},"excerpt":{"rendered":"<p>La cognition sociale est une fonction importante pour de nombreuses esp\u00e8ces qui est alt\u00e9r\u00e9e lors de maladies psychiatriques et neurod\u00e9g\u00e9n\u00e9ratives. Bien que l\u2019hippocampe et en particulier la r\u00e9gion CA2 soient connus pour jouer un r\u00f4le cl\u00e9 dans la formation de m\u00e9moire sociale, les m\u00e9canismes cellulaires impliqu\u00e9s ne sont pas connus. Dans une \u00e9tude r\u00e9cente r\u00e9alis\u00e9e [&hellip;]<\/p>\n","protected":false},"author":4,"featured_media":17526,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[25],"tags":[31],"class_list":["post-17529","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-uncategorized","tag-actualite-en"],"publishpress_future_action":{"enabled":false,"date":"2026-04-22 08:58:53","action":"change-status","newStatus":"draft","terms":[],"taxonomy":"category"},"publishpress_future_workflow_manual_trigger":{"enabledWorkflows":[]},"_links":{"self":[{"href":"https:\/\/www.neurosciences.asso.fr\/en\/wp-json\/wp\/v2\/posts\/17529","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/www.neurosciences.asso.fr\/en\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/www.neurosciences.asso.fr\/en\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/www.neurosciences.asso.fr\/en\/wp-json\/wp\/v2\/users\/4"}],"replies":[{"embeddable":true,"href":"https:\/\/www.neurosciences.asso.fr\/en\/wp-json\/wp\/v2\/comments?post=17529"}],"version-history":[{"count":1,"href":"https:\/\/www.neurosciences.asso.fr\/en\/wp-json\/wp\/v2\/posts\/17529\/revisions"}],"predecessor-version":[{"id":17530,"href":"https:\/\/www.neurosciences.asso.fr\/en\/wp-json\/wp\/v2\/posts\/17529\/revisions\/17530"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/www.neurosciences.asso.fr\/en\/wp-json\/wp\/v2\/media\/17526"}],"wp:attachment":[{"href":"https:\/\/www.neurosciences.asso.fr\/en\/wp-json\/wp\/v2\/media?parent=17529"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/www.neurosciences.asso.fr\/en\/wp-json\/wp\/v2\/categories?post=17529"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/www.neurosciences.asso.fr\/en\/wp-json\/wp\/v2\/tags?post=17529"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}