Calcium Channels and Selective Neuronal Vulnerability in Parkinson’s Disease

Birgit Liss*, D. James Surmeier*

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Scopus citations

Abstract

Ca2+ entry through voltage-dependent ion channels (Cav) in the plasma membrane provides a signal coupling neuronal activity to a wide array of intracellular processes ranging from control of other ion channels to regulation of metabolism and gene expression. In Parkinson’s disease (PD), the degeneration of substantia nigra pars compacta (SNc) dopaminergic neurons, causing the cardinal symptoms, has been tied to the prominent engagement of Cav channels that modulate repetitive spiking, transmitter-release, and mitochondrial function. Here, we summarize the literature underlying this connection. We focus on Cav1 L-type Cav channels, as epidemiological studies indicate that inhibition of these channels reduces the risk of developing PD. In addition, we discuss the translational implications of this literature and the prospect of selective Cav channel modulators as disease-modifying drugs for early-stage PD.

Original languageEnglish (US)
Title of host publicationVoltage-Gated Calcium Channels
PublisherSpringer International Publishing
Pages575-595
Number of pages21
ISBN (Electronic)9783031088810
ISBN (Print)9783031088803
DOIs
StatePublished - Jan 1 2022

Keywords

  • Bioenergetics
  • Ca channel
  • D2 dopamine receptor
  • Dopamine
  • Homeostasis
  • L-type
  • Mitochondria
  • Neurodegeneration
  • Neuronal calcium sensors (NCS)
  • Parkinson’s disease
  • R-type
  • Substantia nigra
  • T-type

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology
  • General Medicine

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