Modulation of K(+)-induced synaptosomal calcium influx by gabapentin

Brain Res. 2000 Sep 1;875(1-2):157-9. doi: 10.1016/s0006-8993(00)02610-x.

Abstract

Gabapentin, a drug useful in several neurological and psychiatric disorders, decreased K(+) (15 mM)-induced [Ca(2+)](i) increase in Fura-PE3-loaded rat neocortical synaptosomes (IC(50)=9.7 microM; submaximal inhibition of 28.6%). This effect may indicate a selective modulation of presynaptic Ca(2+) influx in response to depolarizing (pathological) conditions causing excessive neurotransmitter release.

MeSH terms

  • Acetates / pharmacology*
  • Amines*
  • Animals
  • Calcium / metabolism*
  • Calcium Channel Blockers / administration & dosage
  • Calcium Channel Blockers / pharmacology*
  • Cyclohexanecarboxylic Acids*
  • Dose-Response Relationship, Drug
  • Gabapentin
  • Male
  • Osmolar Concentration
  • Potassium / administration & dosage
  • Potassium / pharmacology
  • Potassium / physiology*
  • Rats
  • Rats, Sprague-Dawley
  • Synaptosomes / metabolism*
  • gamma-Aminobutyric Acid*

Substances

  • Acetates
  • Amines
  • Calcium Channel Blockers
  • Cyclohexanecarboxylic Acids
  • gamma-Aminobutyric Acid
  • Gabapentin
  • Potassium
  • Calcium