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Impact de l’inflammation centrale sur la mémoire

Abstract : The cerebral innate immune system is activated under pathophysiological conditions and can consequently modulate brain functioning and cognitive processes. This modulation is exerted by signals produced by immune-like processes grouped under the term of neuroinflammation and involving neuro-glial communication within the brain. In particular, proinflammatory cytokines and ATP, all produced during this immune system activation have been directly linked to modulation of synaptic plasticity and/or learning and memory functions in animals models. However, the cellular mechanisms by which neuroinflammation modulates neural plasticity and cognitive processes are still unclear. One candidate is the glutamatergic system. Indeed, pro-inflammatory factors can increase or decrease glutamatergic receptors expression and/or activity. Our study was dedicated at deciphering to what extent glutamatergic transmission is altered under neuroinflammation and how this may lead to learning and memory alteration. To this aim, we used the conditioned taste aversion, a task highly dependent on glutamatergic transmission into the insular cortex. Indeed, blockade of NMDA or AMPA receptors in this cortical area before acquisition greatly impairs conditioned taste aversion. The aim of our study was thus to investigate the behavioral and cellular impact of an inflammation restricted to the insular cortex on glutamatergic receptors expression and CTA memory formation. Here we show that a cortical inflammation, induced by LPS infusion into the insular cortex, prior to CTA acquisition enhances the aversion strength presumably through LPS-induced increase of glutamatergic AMPA, but not NMDA, receptor expression/trafficking at the insular synapses. Moreover, we show that ATP release, but not pro-inflammatory cytokines, is responsible for LPS-induced CTA enhancement. In conclusion we propose that inflammation restricted to the insular cortex enhances CTA acquisition through an ATP-dependent mechanism presumably involving an increase of glutamatergic AMPA receptor expression at the neuronal synapses.
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https://hal.inrae.fr/tel-02809292
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Submitted on : Saturday, June 6, 2020 - 6:44:30 AM
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  • HAL Id : tel-02809292, version 1
  • PRODINRA : 194162

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Jean-Christophe Delpech. Impact de l’inflammation centrale sur la mémoire. Sciences du Vivant [q-bio]. Université de Bordeaux Ségalen (Bordeaux 2), 2012. Français. ⟨tel-02809292⟩

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