Fluoxetine Does Not Enhance Visual Perceptual Learning and Triazolam Specifically Impairs Learning Transfer.
The selective serotonin reuptake inhibitor fluoxetine significantly enhances adult visual cortex plasticity within the rat. This effect is related to decreased gamma-aminobutyric acid (GABA) mediated inhibition and identifies fluoxetine as a potential agent for enhancing plasticity in the adult human brain. We tested the hypothesis that fluoxetine would enhance visual perceptual learning of a motion direction discrimination (MDD) task in humans. We also investigated (1) the effect of fluoxetine on visual and motor cortex excitability and (2) the impact of increased GABA mediated inhibition following a single dose of triazolam on post-training MDD task performance. Within a double blind, placebo controlled design, 20 healthy adult participants completed a 19-day course of fluoxetine (n= 10, 20 mg per day) or placebo (n= 10). Participants were trained on the MDD task over the final 5 days of fluoxetine administration. Accuracy for the trained MDD stimulus and an untrained MDD stimulus configuration was assessed before and after training, after triazolam and 1 week after triazolam. Motor and visual cortex excitability were measured using transcranial magnetic stimulation. Fluoxetine did not enhance the magnitude or rate of perceptual learning and full transfer of learning to the untrained stimulus was observed for both groups. After training was complete, trazolam had no effect on trained task performance but significantly impaired untrained task performance. No consistent effects of fluoxetine on cortical excitability were observed. The results do not support the hypothesis that fluoxetine can enhance learning in humans. However, the specific effect of triazolam on MDD task performance for the untrained stimulus suggests that learning and learning transfer rely on dissociable neural mechanisms.
School of Optometry and Vision Science, University of AucklandAuckland, New Zealand; Centre for Brain Research, University of AucklandAuckland, New Zealand.
Alice K
AK
Lagas
School of Optometry and Vision Science, University of AucklandAuckland, New Zealand; Centre for Brain Research, University of AucklandAuckland, New Zealand.
Joanna M
JM
Black
Centre for Brain Research, University of AucklandAuckland, New Zealand; Department of Exercise Sciences, University of AucklandAuckland, New Zealand.
Winston D
WD
Byblow
Department of Exercise Sciences, University of AucklandAuckland, New Zealand; Centre of Human and Aerospace Physiological Sciences, King's College LondonLondon, UK.
Melanie K
MK
Fleming
School of Optometry and Vision Science, University of AucklandAuckland, New Zealand; Centre for Brain Research, University of AucklandAuckland, New Zealand.
Lucy K
LK
Goodman
Centre for Brain Research, University of AucklandAuckland, New Zealand; Department of Psychological Medicine, University of AucklandAuckland, New Zealand.
Robert R
RR
Kydd
School of Pharmacy, University of AucklandAuckland, New Zealand; National School of Pharmacy, University of OtagoDunedin, New Zealand.
Bruce R
BR
Russell
Centre for Brain Research, University of AucklandAuckland, New Zealand; Department of Medicine, University of AucklandAuckland, New Zealand.
Cathy M
CM
Stinear
School of Optometry and Vision Science, University of AucklandAuckland, New Zealand; Centre for Brain Research, University of AucklandAuckland, New Zealand; School of Optometry and Vision Science, University of Waterloo, WaterlooON, Canada.
Benjamin
B
Thompson
TMS; learning; mood; motion perception; motor threshold; paired associative stimulation (PAS); phosphene threshold; serotonin uptake inhibitors