Altered cognitive performance and synaptic function in the hippocampus of mice lacking C3.
(2014) In Experimental Neurology 253. p.154-164- Abstract
- 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 C3 as a negative regulator of the number of functional glutamatergic synapses in the hippocampus. The C3 deficient mice showed no signs... (More)
- 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 C3 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. (Less)
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https://lup.lub.lu.se/record/4292308
- author
- organization
- publishing date
- 2014
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Experimental Neurology
- volume
- 253
- pages
- 154 - 164
- publisher
- Elsevier
- external identifiers
-
- pmid:24378428
- wos:000332055700017
- scopus:84892516407
- pmid:24378428
- ISSN
- 0014-4886
- DOI
- 10.1016/j.expneurol.2013.12.013
- language
- English
- LU publication?
- yes
- id
- 11eef5ec-7ed2-4300-8f73-7df711e2abf1 (old id 4292308)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/24378428?dopt=Abstract
- date added to LUP
- 2016-04-01 10:56:00
- date last changed
- 2022-04-20 07:32:27
@article{11eef5ec-7ed2-4300-8f73-7df711e2abf1, abstract = {{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 C3 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.}}, author = {{Perez-Alcazar, Marta and Daborg, Jonny and Stokowska, Anna and Wasling, Pontus and Björefeldt, Andreas and Kalm, Marie and Zetterberg, Henrik and Carlström, Karl and Blomgren, Klas and Ekdahl Clementson, Christine and Hanse, Eric and Pekna, Marcela}}, issn = {{0014-4886}}, language = {{eng}}, pages = {{154--164}}, publisher = {{Elsevier}}, series = {{Experimental Neurology}}, title = {{Altered cognitive performance and synaptic function in the hippocampus of mice lacking C3.}}, url = {{http://dx.doi.org/10.1016/j.expneurol.2013.12.013}}, doi = {{10.1016/j.expneurol.2013.12.013}}, volume = {{253}}, year = {{2014}}, }