摘要

This paper deals with a new type of access to gating function in the brain, namely the comparison of the N100 auditory responses to an overt tone burst, and its inhibition when paired with a weak (i.e. auditory click but small in amplitude) pre-pulse. A beginning of neuropharmacological characterisation has been made in healthy subjects in order to get a hand on a potential clinical application elaborating the most advanced mechanistic basis for negative symptoms in schizophrenia.
The first part of this paper is meant to set the conditions and to demonstrate the involvement of NMDA receptors. Thereafter previous results concerning disruption of the gating function of the N100 could be confirmed and relevant examples of preliminary individual findings of controlled administration of psychotomimetic doses of ketamine has been inferred (case 1). Still at the individual level high and low doses of ketamine distinguisheds responses neuropharmacologically (case 2). The final aim has been to test the capability of a positive modulator of glutamate receptors to block the disruptive effect of ketamine. To this end volunteers have been pre-loaded for 2 days with a naturally occurring aminoacid, glycine, which is a co-agonist for the NMDA receptor; the effects on gating function of the N100 during the ketamine challenge were partially succesfull (case 3) and have succinctly been reported.

  • 出版日期2008