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The complement inhibitor CD59 is required for GABAergic synaptic transmission in the dentate gyrus

Lang Wen1, Xiaoli Yang1, Zujun Wu1

  • 1Department of Neurology and Institute on Aging and Brain Disorders, The First Affiliated Hospital of USTC, Neurodegenerative Disease Research Center, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230026, China.

Cell Reports
|April 7, 2023
PubMed

Insights

Loss of CD59, a complement inhibitor, impairs spatial memory and hippocampal inhibitory function. This study reveals CD59 regulates GABA release, not synaptic pruning, in the brain.

Area of Science:

  • Neuroscience
  • Immunology
  • Molecular Biology

Background:

  • Microglia-mediated complement-dependent pruning of excitatory synapses is known.
  • Limited understanding exists regarding complement's role in inhibitory synapses and synaptic transmission.

Purpose of the Study:

  • To investigate the role of CD59, a complement inhibitor, in synaptic function and memory.
  • To elucidate the mechanism by which CD59 deficiency affects hippocampal synaptic transmission.

Main Methods:

  • Spatial memory performance tests in CD59-deficient models.
  • Electrophysiological recordings in the hippocampal dentate gyrus (DG).
  • Analysis of GABAergic synaptic transmission and SNARE complex assembly.

Main Results:

  • CD59 deficiency resulted in impaired spatial memory.
  • GABAergic synaptic transmission was compromised in the DG of CD59-deficient mice.
  • CD59 regulates GABA release via modulation of Ca2+ influx and SNARE complex assembly, independent of microglial pruning.

Conclusions:

  • The complement regulator CD59 is crucial for normal hippocampal function.
  • CD59 plays a direct role in regulating inhibitory synaptic transmission.
  • CD59's function extends beyond complement inhibition to direct synaptic regulation.
Keywords:
CD59CP: Neurosciencecomplementdentate gyrushippocampuslearning and memorymicroglia engulfmentsynaptic transmission

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