ArticleThe Journal of biological chemistry2015
L-type Calcium Channel Cav1.2 Is Required for Maintenance of Auditory Brainstem Nuclei.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- Neurotransmitters in Auditory Processing Disorders and Neurodevelopmental Disorders: A Common Neurobiological Substrate?Children (Basel, Switzerland) · 2026Review
- L-type calcium channel modulation reveals the relationship between neuronal synchrony and hyperactivity in the inferior colliculus following noise-induced hearing loss.Scientific reports · 2025Article
- Pre-Sensory Spontaneous Activity Accelerates Coordinated Maturation of Synaptic Partners and Drives Transition to the Mature Physiological Phenotype.bioRxiv : the preprint server for biology · 2025Article
- Maintenance of a central high frequency synapse in the absence of synaptic activity.Frontiers in cellular neuroscience · 2024Article
- Serine 937 phosphorylation enhances KCC2 activity and strengthens synaptic inhibition.Scientific reports · 2023Article
- Shared and organ-specific gene-expression programs during the development of the cochlea and the superior olivary complex.RNA biology · 2023Article
- Expression pattern of cochlear microRNAs in the mammalian auditory hindbrain.Cell and tissue research · 2021Article
- Article
- Effects of Neurotrophin-3 on Intrinsic Neuronal Properties at a Central Auditory Structure.Neuroscience insights · 2020Article
- Activity-dependent formation of a vesicular inhibitory amino acid transporter gradient in the superior olivary complex of NMRI mice.BMC neuroscience · 2017Article
- In vivo matching of postsynaptic excitability with spontaneous synaptic inputs during formation of the rat calyx of Held synapse.The Journal of physiology · 2017Article
- Functional Role of γ-Crystallin N in the Auditory Hindbrain.PloS one · 2016Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cav1.2 and Cav1.3 are the major L-type voltage-gated Ca(2+) channels in the CNS. Yet, their individual in vivo functions are largely unknown. Both channel subunits are expressed in the auditory brainstem, where Cav1.3 is essential for proper maturation. Here, we investigated the role of Cav1.2 by targeted deletion in the mouse embryonic auditory brainstem. Similar to Cav1.3, loss of Cav1.2 resulted in a significant decrease in the volume and cell number of auditory nuclei. Contrary to the deletion of Cav1.3, the action potentials of lateral superior olive (LSO) neurons were narrower compared with controls, whereas the firing behavior and neurotransmission appeared unchanged. Furthermore, auditory brainstem responses were nearly normal in mice lacking Cav1.2. Perineuronal nets were also unaffected. The medial nucleus of the trapezoid body underwent a rapid cell loss between postnatal days P0 and P4, shortly after circuit formation. Phosphorylated cAMP response element-binding protein (CREB), nuclear NFATc4, and the expression levels of p75NTR, Fas, and FasL did not correlate with cell death. These data demonstrate for the first time that both Cav1.2 and Cav1.3 are necessary for neuronal survival but are differentially required for the biophysical properties of neurons. Thus, they perform common as well as distinct functions in the same tissue.
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