Altered cognitive performance and synaptic function in the hippocampus of mice lacking C3
Copyright policy )Altered cognitive performance and synaptic function in the hippocampus of mice lacking C3
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.
- University of Gothenburg Sweden
- University of Melbourne Australia
- Karolinska Institute Sweden
- University College London United Kingdom
- Skåne University Hospital Sweden
Male, Development, In Vitro Techniques, Hippocampus, GABA Antagonists, Mice, Developmental Neuroscience, Synapse elimination, Avoidance Learning, Animals, Mice, Knockout, Neurons, Epilepsy, Excitatory Postsynaptic Potentials, Complement C3, Electric Stimulation, Complement cascade, Mice, Inbred C57BL, Disease Models, Animal, Neurology, Animals, Newborn, Gene Expression Regulation, Dizocilpine Maleate, Nerve Net, Cognition Disorders, Excitatory Amino Acid Antagonists
Male, Development, In Vitro Techniques, Hippocampus, GABA Antagonists, Mice, Developmental Neuroscience, Synapse elimination, Avoidance Learning, Animals, Mice, Knockout, Neurons, Epilepsy, Excitatory Postsynaptic Potentials, Complement C3, Electric Stimulation, Complement cascade, Mice, Inbred C57BL, Disease Models, Animal, Neurology, Animals, Newborn, Gene Expression Regulation, Dizocilpine Maleate, Nerve Net, Cognition Disorders, Excitatory Amino Acid Antagonists
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