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Molecular pathways underlying the modulation of T-type calcium channels by neurotransmitters and hormones

Jean Chemin1, Achraf Traboulsie, Philippe Lory

  • 1Département de Physiologie, Institut de Génomique Fonctionnelle (IGF), CNRS UMR 5203 - INSERM U661 - Universités de Montpellier I & II, 141 rue de la Cardonille, 34094 Montpellier, France. jean.chemin@igf.cnrs.fr

Cell Calcium
|June 27, 2006
PubMed

Insights

Neurotransmitters and hormones modulate T-type calcium channels, crucial for brain function and epilepsy. This review clarifies the roles of G proteins and protein kinases in these short-term regulatory effects.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pharmacology

Background:

  • Low-voltage-activated T-type calcium channels (TCCs) are vital in the brain, influencing neuronal firing, sleep, and epilepsy.
  • Mechanisms of TCC modulation by hormones and neurotransmitters are less understood compared to high-voltage-activated channels.
  • Existing data on TCC regulation by various signaling molecules show inconsistencies across different cell types.

Purpose of the Study:

  • To review the short-term (minutes) modulation of T-type calcium channels by hormones and neurotransmitters.
  • To elucidate the involvement of G proteins and protein kinases in TCC regulation.
  • To compare findings from native tissues with studies on cloned TCCs (CaV3.1, CaV3.2, CaV3.3).

Main Methods:

  • Literature review focusing on short-term modulation studies.
  • Analysis of data from various native tissues expressing TCCs.
  • Comparison with studies utilizing expression systems for cloned TCCs.

Main Results:

  • Hormones and neurotransmitters exert short-term control over T-type calcium channel activity.
  • G proteins and protein kinases play significant roles in mediating these modulatory effects.
  • Discrepancies in modulation effects highlight cell-type-specific regulation.

Conclusions:

  • Understanding TCC modulation is critical for neurological disorders like absence epilepsy.
  • G protein-coupled receptors and kinase pathways are key regulators of TCC function.
  • Further research is needed to reconcile cell-specific differences in TCC modulation.

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