Release of [(3)H]-L-glutamate by stimulation of nicotinic acetylcholine receptors in rat cerebellar slices

Neuroscience. 2004;124(3):647-53. doi: 10.1016/j.neuroscience.2003.12.023.

Abstract

This is a neurochemical study which shows that nicotine acting through alpha7-containing nicotinic acetylcholine receptors promotes the release of [(3)H]-glutamate from rat cerebellar slices. Release evoked by half maximal concentration of nicotine (100 microM) was blocked by alpha-bungarotoxin and in a calcium-free medium, suggesting an effect mediated by an alpha7 receptor. Dihydro-beta-erythroidine and mecamylamine were effective only at very high concentrations, excluding the participation of heteromeric receptors. The effect of nicotine was partially blocked by inhibitors of glutamatergic receptors DL-2-amino-5-phosphonovaleric acid and 6-cyano-7-nitroquinoxaline-2,3-dione, indicating a glutamate-induced glutamate release. Nicotine-evoked response was dependent on activation of tetrodotoxin sensitive sodium channels. Therefore, here we show that glutamate released by stimulation of alpha7-containing nicotinic receptors, located preterminal and/or postsynaptically, evokes a further glutamate release in adult rat cerebellar slices.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cerebellum / drug effects
  • Cerebellum / metabolism*
  • Excitatory Amino Acid Antagonists / pharmacology
  • Glutamic Acid / metabolism*
  • In Vitro Techniques
  • Male
  • Nicotine / pharmacology
  • Nicotinic Antagonists / pharmacology
  • Potassium Chloride / pharmacology
  • Presynaptic Terminals / drug effects
  • Presynaptic Terminals / metabolism*
  • Rats
  • Receptors, Glutamate / drug effects
  • Receptors, Glutamate / metabolism
  • Receptors, Nicotinic / drug effects
  • Receptors, Nicotinic / metabolism*
  • Sodium Channels / drug effects
  • Sodium Channels / metabolism
  • Stimulation, Chemical
  • Synaptic Membranes / drug effects
  • Synaptic Membranes / metabolism
  • Synaptic Transmission / drug effects
  • Synaptic Transmission / physiology*
  • Tritium
  • alpha7 Nicotinic Acetylcholine Receptor

Substances

  • Chrna7 protein, rat
  • Excitatory Amino Acid Antagonists
  • Nicotinic Antagonists
  • Receptors, Glutamate
  • Receptors, Nicotinic
  • Sodium Channels
  • alpha7 Nicotinic Acetylcholine Receptor
  • Tritium
  • Glutamic Acid
  • Potassium Chloride
  • Nicotine