Inhibition by anandamide and synthetic cannabimimetics of the release of [3H] D- aspartate and [3H] GABA from synaptosomes isolated from the rat hippocampus

Carla Cannizzaro, Preziosi, Maria Martire, D'Amico

Risultato della ricerca: Article

20 Citazioni (Scopus)

Abstract

Cannabinoids (CB) can act as retrograde synaptic mediators of depolarization-induced suppression of inhibition or excitation in hippocampus. This mechanism may underlie the impairment of some cognitive processes produced by these compounds, including short-term memory formation in the hippocampus. In this study, we investigated several compounds known to interact with CB receptors, evaluating their effects on K +-evoked release of [ 3H]d-aspartate ([ 3H]d-ASP) and [ 3H]GABA from superfused synaptosomes isolated from the rat hippocampus. [ 3H]d-ASP and [ 3H]GABA release were inhibited to different degrees by the synthetic cannabinoids WIN 55,212-2; CP 55,940, and arachidonyl-2′- chloroethylamide/N-(2-chloroethyl)-5Z,8Z,11Z,14Z-eicosatetraenamide (ACEA), as well as by the endocannabinoids, anandamide (AEA), and 2-arachidonoylglycerol (2-AG). Both types of release were also inhibited by capsaicin. The inhibition produced by each of the cannabinoid compounds and capsaicin was unaffected by capsazepine or by the CB1-receptor antagonists AM-251 and SR141716A. The mechanism underlying AEA- and synthetic CB-induced inhibition of the release of [ 3H]GABA and [ 3H]d-ASP from rat hippocampal synaptosomes might not involve activation of presynaptic CB1 receptors.
Lingua originaleEnglish
pagine (da-a)1553-1561
Numero di pagine9
RivistaNeurochemical Research
Volume29
Stato di pubblicazionePublished - 2004

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Cellular and Molecular Neuroscience

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