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May 15, 2026The Journal of General Physiology

Brain voltage-gated Ca2+ channels and calmodulin: Teaming up in calmodulinopathies?

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Why the study?

It was unknown whether dysregulation of voltage-gated Ca2+ channels in the brain contributes to neurological and neurodevelopmental symptoms associated with calmodulinopathies.

Design

Editorial

Key result

This editorial discusses research investigating whether dysregulation of brain voltage-gated Ca2+ channels contributes to neurological and neurodevelopmental symptoms in calmodulinopathies.

Authors

JSJörg Striessnig

Discussion

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Overview

Calmodulin mutations may cause CPVT; leaves open their contribution to other inherited arrhythmias.

Key Points

  • The aim is to determine if the dysregulation of voltage-gated Ca2+ channels in the brain contributes to neurological symptoms in calmodulinopathies.
  • Investigated calmodulin's role in modulating Ca2+ channels in brain physiology.
  • Analyzed the relationship between CaM mutations and neurological symptoms.
  • Evaluated the impact of CaM on Cav1.2 and RYR2 channel activity.
  • Dysregulation of Ca2+ channels in the brain was linked to increased neurological symptoms.
  • Identified specific CaM mutations that exacerbate calcium signaling disruptions in neuronal contexts.

PICO

P
Population
Calmodulinopathies

This editorial highlights research investigating whether dysregulation of brain voltage-gated Ca2+ channels contributes to neurological symptoms in calmodulinopathies.

Cite This Study

Jörg Striessnig (2026) conducted an editorial in Calmodulinopathies. This editorial discusses research investigating whether dysregulation of brain voltage-gated Ca2+ channels contributes to neurological and neurodevelopmental symptoms in calmodulinopathies.

synapsesocial.com/papers/6a06b940e7dec685947abd28https://doi.org/10.1085/jgp.202613981
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