NMDA receptor-dependent long-term potentiation is dependent on low-voltage-activated calcium currents in the sensorimotor cortex of cats

Brain Res. 2004 May 15;1008(1):116-9. doi: 10.1016/j.brainres.2004.01.024.

Abstract

The role of low-voltage-activated (LVA) calcium channels in the expression of long-term potentiation (LTP) was examined by intracellular recording in slices from cat agranular cortex. In the normal solution, LTP was induced, and the potentiation of low-threshold rebound potential was evoked by negative current injection. In the cells, in which resting membrane potential was depolarized, the incidence of LTP was very low. LTP was blocked completely in the presence of NMDA receptor antagonist or 50-100 microM nickel. It was suggested that LVA calcium channels function downstream of NMDA receptor-dependent signaling.

Publication types

  • Comparative Study

MeSH terms

  • 2-Amino-5-phosphonovalerate / pharmacology
  • Animals
  • Calcium Channels / drug effects
  • Calcium Channels / physiology*
  • Cats
  • Dose-Response Relationship, Drug
  • Drug Interactions
  • Excitatory Amino Acid Antagonists / pharmacology
  • In Vitro Techniques
  • Long-Term Potentiation / drug effects
  • Long-Term Potentiation / physiology*
  • Motor Cortex / drug effects
  • Motor Cortex / physiology*
  • Nickel / pharmacology
  • Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors
  • Receptors, N-Methyl-D-Aspartate / physiology*
  • Somatosensory Cortex / drug effects
  • Somatosensory Cortex / physiology*

Substances

  • Calcium Channels
  • Excitatory Amino Acid Antagonists
  • Receptors, N-Methyl-D-Aspartate
  • 2-Amino-5-phosphonovalerate
  • Nickel