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Assessment of serotonin function, memory and spatial working memory using buspirone and placebo

Published online by Cambridge University Press:  24 June 2014

D Piskulic,
J Olver,
P Maruff and
T Norman
D Piskulic
Affiliation:
The University of Melbourne, Melbourne, AustraliaAustin Health
J Olver
Affiliation:
The University of Melbourne, Melbourne, AustraliaAustin Health
P Maruff
Affiliation:
CogState Ltd, Melbourne, Australia
T Norman
Affiliation:
The University of Melbourne, Melbourne, AustraliaAustin Health
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Abstract

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Information

Type
Abstracts from ‘Brainwaves’— The Australasian Society for Psychiatric Research Annual Meeting 2006, 6–8 December, Sydney, Australia
Information
Acta Neuropsychiatrica , Volume 18 , Issue 6 , December 2006, pp. 303 - 304
Copyright
Copyright © 2006 Blackwell Munksgaard

Introduction:

The neurotransmitters serotonin and dopamine are implicated in normal cognitive functioning. In healthy volunteers, dopamine depletion produces selective deficits of spatial working memory (SWM) while serotonin depletion results in deficits on a delayed word recall task (delayed verbal learning). Serotonin 5-HT1A receptors in man are found in post-synaptic locations in hippocampus and neocortex, and as somatodendritic autoreceptors in the raphe nuclei. 5-HT1A agonists have been shown to preferentially increase dopamine in the prefrontal cortex (PFC) acting by means of the 5-HT1A autoreceptors, which may influence cognitive function and memory in particular. We aimed to investigate the relationship between serotonin activity and memory performance in healthy volunteers.

Method:

Ten male and 10 female healthy volunteers (aged between 18 and 60 years) were tested in a randomized, double-blind, crossover design receiving both buspirone (20 mg) and placebo over the course of the study. All subjects completed tests of reaction time, SWM and verbal learning.

Results:

Repeated-measures ANOVA showed significant decrement in delayed word recall performance after buspirone administration. SWM and RT data will be available for discussion at the time of presentation.

Conclusions:

Single dose of buspirone caused slight but nonetheless significant worsening in delayed verbal recall in healthy volunteers. This outcome may be because of 1) verbal memory decrements as a result of nondirect 5-HT1A receptor action on dopamine function in the PFC or, alternatively, 2) buspirone-induced changes in serotonergic function in the hippocampus.