期刊
EXPERIMENTAL NEUROLOGY
卷 253, 期 -, 页码 154-164出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.expneurol.2013.12.013
关键词
Complement cascade; Development; Epilepsy; Hippocampus; Synapse elimination
资金
- Swedish Research Council [20116, 12600, 14250, 21562]
- ALF Goteborg [142821, 13699, 144341]
- ALF Lund
- Hjamfonden
- Goteborg Foundation for Neurological Research
- U. and R. Amlov's Foundation
- E. Jacobson's Donation Fund
- Sten A. Olsson Foundation for Research and Culture
- W. and M. Lundgren's Foundation
- Alzheimer's Foundation
- Swedish Childhood Cancer Foundation (Barncancerfonden)
- King Gustav V Jubilee Clinic Cancer Research Foundation (JK-fonden)
- Frimurare Barnhus Foundation
- Gothenburg Medical Society
- Sahlgrenska Foundations
- Swedish Society of Medicine
Previous work implicated the complement system in adult neurogenesis as well as elimination of synapses in the developing and injured CNS. In the present study, we used mice lacking the third complement component (C3) to elucidate the role the complement system plays in hippocampus-dependent learning and synaptic function. We found that the constitutive absence of C3 is associated with enhanced place and reversal learning in adult mice. Our findings of lower release probability at CA3-CA1 glutamatergic synapses in combination with unaltered overall efficacy of these synapses in C3 deficient mice implicate 0 as a negative regulator of the number of functional glutamatergic synapses in the hippocampus. The C3 deficient mice showed no signs of spontaneous epileptiform activity in the hippocampus. We conclude that C3 plays a role in the regulation of the number and function of glutamatergic synapses in the hippocampus and exerts negative effects on hippocampus-dependent cognitive performance. (C) 2014 The Authors. Published by Elsevier Inc. All rights reserved.
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