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Loss of C1q alters the auditory brainstem response
Sima M Chokr1, Ashley Bui-Tran1, Karina S Cramer1
1Department of Neurobiology and Behavior, University of California Irvine, Irvine, CA, United States.
Frontiers in Cellular Neuroscience
|October 17, 2024
Summary
The complement protein C1q is present in the auditory brainstem during development. C1q deficiency in mice subtly impacts auditory brainstem response (ABR) peak latencies without affecting hearing thresholds or synaptic pruning.
Area of Science:
- Neuroscience
- Auditory system development
- Synaptic plasticity
Background:
- Neural circuits in the auditory brainstem, specifically the ventral cochlear nucleus (VCN) and medial nucleus of the trapezoid (MNTB), are crucial for sound localization.
- Microglia play a role in synaptic pruning, as evidenced by impaired pruning and auditory brainstem responses (ABRs) when microglia are inhibited.
- The C1q-initiated complement cascade is a known microglial pathway involved in synaptic pruning and plasticity.
Purpose of the Study:
- To investigate the role of the classical complement pathway initiator, C1q, in auditory brainstem maturation.
- To determine the developmental expression pattern of C1q in the sound localization pathway.
- To assess the functional consequences of C1q deletion on auditory brainstem function and synaptic development.
Main Methods:
- Investigated C1q expression in the MNTB during postnatal development in mice.
- Analyzed C1q localization within microglia and around MNTB principal neurons.
- Assessed the impact of C1q deletion on microglia-dependent calyceal pruning, synaptic markers, and ABRs in C1q knockout (KO) mice.
Main Results:
- C1q expression was detected in the MNTB by the first postnatal week, increasing with age.
- C1q was found within microglia and surrounding MNTB principal neurons.
- C1q deletion did not affect microglia-dependent calyceal pruning or alter synaptic markers in the MNTB and LSO. C1q KO mice exhibited normal hearing thresholds but shortened ABR peak latencies.
Conclusions:
- This study establishes the developmental timeline of C1q expression within the auditory brainstem's sound localization pathway.
- Loss of C1q leads to subtle functional changes in auditory processing, specifically shortened ABR peak latencies, without compromising basic hearing or synaptic pruning mechanisms.
- C1q plays a nuanced role in auditory brainstem maturation, distinct from its previously observed effects when microglia are broadly inhibited.
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