PubMed 25698740
Referenced in: none
Automatically associated channels: TASK1
Title: Microglial activation enhances associative taste memory through purinergic modulation of glutamatergic neurotransmission.
Authors: Jean-Christophe Delpech, Nicolas Saucisse, Shauna L Parkes, Chloe Lacabanne, Agnès Aubert, Fabrice Casenave, Etienne Coutureau, Nathalie Sans, Sophie Layé, Guillaume Ferreira, Agnès Nadjar
Journal, date & volume: J. Neurosci., 2015 Feb 18 , 35, 3022-33
PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/25698740
Abstract
The cerebral innate immune system is able to modulate brain functioning and cognitive processes. During activation of the cerebral innate immune system, inflammatory factors produced by microglia, such as cytokines and adenosine triphosphate (ATP), have been directly linked to modulation of glutamatergic system on one hand and learning and memory functions on the other hand. However, the cellular mechanisms by which microglial activation modulates cognitive processes are still unclear. Here, we used taste memory tasks, highly dependent on glutamatergic transmission in the insular cortex, to investigate the behavioral and cellular impacts of an inflammation restricted to this cortical area in rats. We first show that intrainsular infusion of the endotoxin lipopolysaccharide induces a local inflammation and increases glutamatergic AMPA, but not NMDA, receptor expression at the synaptic level. This cortical inflammation also enhances associative, but not incidental, taste memory through increase of glutamatergic AMPA receptor trafficking. Moreover, we demonstrate that ATP, but not proinflammatory cytokines, is responsible for inflammation-induced enhancement of both associative taste memory and AMPA receptor expression in insular cortex. In conclusion, we propose that inflammation restricted to the insular cortex enhances associative taste memory through a purinergic-dependent increase of glutamatergic AMPA receptor expression at the synapse.