High-dose glycine inhibits the loudness dependence of the auditory evoked potential (LDAEP) in healthy humans

Abstract

While the exact mechanism responsible for the effects of glycine on the LDAEP are not known, the findings suggest an inhibitory effect in the cortex, possibly via activation of NMDA receptors on GABA interneurons or inhibitory glycine receptors. The findings add to the growing literature exhibiting modulation of the LDAEP by multiple neurochemical systems in addition to the serotonergic system.

Effects of selective and combined serotonin and dopamine depletion on the loudness dependence of the auditory evoked potential (LDAEP) in humans

“…Dipole source analysis (DSA) was not utilized with the LDAEP examined only from the C Z electrode, a method used previously in a number of studies (Croft et al, 2001;Gallinat et al, 2003;Lee et al, 2005;Nathan et al, 2006;O'Neill et al, 2006O'Neill et al, , 2007. However, as yet, the advantage of DSA in comparison to measurement from C Z has not been shown, with similar results reported using both methods (Croft et al, 2001;Tuchtenhagen et al, 2000).…”

Chronic modulation of serotonergic neurotransmission with sertraline attenuates the loudness dependence of the auditory evoked potential in healthy participants

“…However, there is evidence that the LDAEP is modulated by systems other than the indicated serotonergic involvement (Pogarell et al 2004;O'Neill et al 2006O'Neill et al , 2007Juckel et al 2008c). Sertraline has an affinity for DA transporter (DAT) reuptake inhibition, in fact the highest affinity of all the SSRIs (Hyttel 1994;Owens et al 2001 ) has been reported to influence the LDAEP; however, a preliminary study has reported a significant relationship between genetic variants of the COMT gene influencing synaptic DA levels and the LDAEP (Juckel et al 2008c).…”

“…This has included studies examining the acute effects of SSRIs in healthy participants (Uhl et al 2006;Guille et al 2008). Indeed, some studies have reported evidence indicating that the LDAEP is not only determined by serotonergic function, with both synaptic dopamine (DA) reuptake transporter availability (Pogarell et al 2004) and DA inactivation (via the COMT enzyme; Juckel et al 2008c), BDNF levels (Lang et al 2005) and N-methyl-D-aspartate (NMDA) receptors (O'Neill et al 2007) implicated. This raises the question of whether the LDAEP is a reliable indicator of serotonergic function in humans.…”

How Human Electrophysiology Informs Psychopharmacology: from Bottom-up Driven Processing to Top-Down Control

“…O'Neill et al (2007) also studied the effects of high-dose glycine, a modulator of NMDA receptors on LDAEP. They showed a weaker LDAEP (a pronounced decrease in the slope of the N1/P2 with increasing tone loudness) after glycine administration.…”