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Related Experiment Video

Updated: Jan 2, 2026

Monocular Visual Deprivation and Ocular Dominance Plasticity Measurement in the Mouse Primary Visual Cortex
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Ocular Dominance Plasticity in Binocular Primary Visual Cortex Does Not Require C1q.

Christina A Welsh1, Céleste-Élise Stephany1, Richard W Sapp2

  • 1F.M. Kirby Neurobiology Center, Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|December 6, 2019
PubMed
Summary

Complement component C1q is not essential for visual cortex development or ocular dominance plasticity in mice. Despite its role in synapse elimination, C1q deficiency did not impair visual system refinement or neuronal responsiveness.

Keywords:
C1qclassical complement cascadeneural-immune interactionsocular dominance plasticitysynapse eliminationvisual cortex

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Area of Science:

  • Neuroscience
  • Immunology
  • Developmental Biology

Background:

  • C1q initiates the classical complement cascade and mediates synapse elimination in early development.
  • The visual cortex (V1b) undergoes experience-dependent synaptic refinement during a critical period, known as ocular dominance plasticity (ODP).

Purpose of the Study:

  • To investigate the role of C1q in experience-dependent synaptic refinement in the mouse visual system at later developmental stages.
  • To determine if ocular dominance plasticity (ODP) and V1b development are impaired in mice lacking C1q.

Main Methods:

  • Analysis of V1b development in mice genetically engineered to lack C1q.
  • Assessment of spine densities, dendritic morphologies, neuronal firing rates, and ocular dominance shifts following eye closure.
  • Experiments conducted on both male and female mice.

Main Results:

  • Mice lacking C1q exhibited normal V1b development, including spine densities on most dendrites, firing rates, and ocular dominance.
  • C1q was transiently required only for spine development on specific apical dendrites, not basal ones.
  • Despite the absence of expected spine loss during ODP, C1q-deficient mice showed normal shifts in neuronal responsiveness after eye closure.

Conclusions:

  • The development and experience-dependent plasticity of the mouse V1b are largely normal in the absence of C1q.
  • C1q's role in synapse elimination appears context-dependent, with less impact on V1b plasticity compared to other brain regions like the thalamus or hippocampus.