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

CX3CR1 Deficiency Leads to Impairment of Hippocampal Cognitive Function and Synaptic Plasticity The Journal of Neuroscience, November 9, 2011 • 31(45):16241–16250 • 16241 Development/Plasticity/Repair CX3CR1 Deficiency Leads to Impairment of Hippocampal Cognitive Function and Synaptic Plasticity 1 2 2 3 1 Justin T. Rogers, * Josh M. Morganti, * Adam D. Bachstetter, Charles E. Hudson, Melinda M. Peters, 2 1 2,3 2,3 Bethany A. Grimmig, Edwin J. Weeber, Paula C. Bickford, and Carmelina Gemma 1 2 Department of Molecular Pharmacology and Physiology, USF Health Byrd Alzheimer’s Institute and Department of Neurosurgery and Brain Repair, University of South Florida, Tampa, Florida 33612, and James A. Haley Veterans Affairs’ Medical Center, Tampa FL, 33612 The protective/neurotoxic role of fractalkine (CX3CL1) and its receptor CX3C chemokine receptor 1 (CX3CR1) signaling in neurodegen- erative disease is an intricate and highly debated research topic and it is becoming even more complicated as new studies reveal discordant results. It appears that the CX3CL1/CX3CR1 axis plays a direct role in neurodegeneration and/or neuroprotection depending on the CNS insult. However, all the above studies focused on the role of CX3CL1/CX3CR1 signaling in pathological conditions, ignoring the relevance of CX3CL1/CX3CR1 signaling under physiological conditions. No approach to date has been taken to decipher the significance / / of defects in http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neuroscience Unpaywall

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

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Publisher
Unpaywall
ISSN
0270-6474
DOI
10.1523/jneurosci.3667-11.2011
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Abstract

The Journal of Neuroscience, November 9, 2011 • 31(45):16241–16250 • 16241 Development/Plasticity/Repair CX3CR1 Deficiency Leads to Impairment of Hippocampal Cognitive Function and Synaptic Plasticity 1 2 2 3 1 Justin T. Rogers, * Josh M. Morganti, * Adam D. Bachstetter, Charles E. Hudson, Melinda M. Peters, 2 1 2,3 2,3 Bethany A. Grimmig, Edwin J. Weeber, Paula C. Bickford, and Carmelina Gemma 1 2 Department of Molecular Pharmacology and Physiology, USF Health Byrd Alzheimer’s Institute and Department of Neurosurgery and Brain Repair, University of South Florida, Tampa, Florida 33612, and James A. Haley Veterans Affairs’ Medical Center, Tampa FL, 33612 The protective/neurotoxic role of fractalkine (CX3CL1) and its receptor CX3C chemokine receptor 1 (CX3CR1) signaling in neurodegen- erative disease is an intricate and highly debated research topic and it is becoming even more complicated as new studies reveal discordant results. It appears that the CX3CL1/CX3CR1 axis plays a direct role in neurodegeneration and/or neuroprotection depending on the CNS insult. However, all the above studies focused on the role of CX3CL1/CX3CR1 signaling in pathological conditions, ignoring the relevance of CX3CL1/CX3CR1 signaling under physiological conditions. No approach to date has been taken to decipher the significance / / of defects in

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Journal of Neuroscience – Unpaywall

Published: Nov 9, 2011

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