Functional expression of T-type Ca2+ channels in spinal motoneurons of the adult turtle

PLoS One. 2014 Sep 25;9(9):e108187. doi: 10.1371/journal.pone.0108187. eCollection 2014.

Abstract

Voltage-gated Ca2+ (CaV) channels are transmembrane proteins comprising three subfamilies named CaV1, CaV2 and CaV3. The CaV3 channel subfamily groups the low-voltage activated Ca2+ channels (LVA or T-type) a significant role in regulating neuronal excitability. CaV3 channel activity may lead to the generation of complex patterns of action potential firing such as the postinhibitory rebound (PIR). In the adult spinal cord, these channels have been found in dorsal horn interneurons where they control physiological events near the resting potential and participate in determining excitability. In motoneurons, CaV3 channels have been found during development, but their functional expression has not yet been reported in adult animals. Here, we show evidence for the presence of CaV3 channel-mediated PIR in motoneurons of the adult turtle spinal cord. Our results indicate that Ni2+ and NNC55-0396, two antagonists of CaV3 channel activity, inhibited PIR in the adult turtle spinal cord. Molecular biology and biochemical assays revealed the expression of the CaV3.1 channel isotype and its localization in motoneurons. Together, these results provide evidence for the expression of CaV3.1 channels in the spinal cord of adult animals and show also that these channels may contribute to determine the excitability of motoneurons.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium Channel Blockers / pharmacology
  • Calcium Channels, T-Type / genetics*
  • Calcium Channels, T-Type / metabolism
  • Gene Expression*
  • Membrane Potentials
  • Motor Neurons / drug effects
  • Motor Neurons / metabolism*
  • Spinal Cord / cytology*
  • Spinal Cord / metabolism*
  • Turtles

Substances

  • Calcium Channel Blockers
  • Calcium Channels, T-Type

Grant support

This work was supported by grants from the National Council of Science and Technology (Conacyt) of Mexico to R. F. and R. D.- L. (128707-Q and 50864-Q, respectively). The URL of the funder is http://www.conacyt.mx/. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.