CX3CR1 Deficiency Leads to Impairment of Hippocampal Cognitive Function and Synaptic Plasticity

• DOI: 10.1523/jneurosci.3667-11.2011
• Publication Date: 2011-11-09T17:51:06Z
• Authors: Justin T. Rogers; Josh M. Morganti; Adam D. Bachstetter; Charles E. Hudson; Melinda M. Peters; Bethany A. Grimmig; Edwin J. Weeber; Paula C. Bickford; Carmelina Gemma
• Keywords: CX3CR1; CX3CL1

The protective/neurotoxic role of fractalkine (CX3CL1) and its receptor CX3C chemokine 1 (CX3CR1) signaling in neurodegenerative disease is an intricate highly debated research topic it becoming even more complicated as new studies reveal discordant results. It appears that the CX3CL1/CX3CR1 axis plays a direct neurodegeneration and/or neuroprotection depending on CNS insult. However, all above focused pathological conditions, ignoring relevance under physiological conditions. No approach to date has been taken decipher significance defects condition. In present study we used CX3CR1 −/− , +/− wild-type mice investigate cognition synaptic plasticity. Our results demonstrate for first time lacking show contextual fear conditioning Morris water maze deficits. deficiency also affects motor learning. Importantly, have significant impairment long-term potentiation (LTP). Infusion with IL-1β antagonist significantly reversed deficit cognitive function LTP. disruption CX3CL1 will lead plasticity via increased action IL-1β.