posted on 2016-04-29, 00:00authored byBruno Campos, Claudia Rivetti, Timm Kress, Carlos Barata, Heinrich Dircksen
Selective
serotonin reuptake inhibitors (SSRIs) are widely used
antidepressants. As endocrine disruptive contaminants in the environment,
SSRIs affect reproduction in aquatic organisms. In the water flea Daphnia magna, SSRIs increase offspring production
in a food ration-dependent manner. At limiting food conditions, females
exposed to SSRIs produce more but smaller offspring, which is a maladaptive
life-history strategy. We asked whether increased serotonin levels
in newly identified serotonin-neurons in the Daphnia brain mediate these effects. We provide strong evidence that exogenous
SSRI fluoxetine selectively increases serotonin-immunoreactivity in
identified brain neurons under limiting food conditions thereby leading
to maladaptive offspring production. Fluoxetine increases serotonin-immunoreactivity
at low food conditions to similar maximal levels as observed under
high food conditions and concomitantly enhances offspring production.
Sublethal amounts of the neurotoxin 5,7-dihydroxytryptamine known
to specifically ablate serotonin-neurons markedly decrease serotonin-immunoreactivity
and offspring production, strongly supporting the effect to be serotonin-specific
by reversing the reproductive phenotype attained under fluoxetine.
Thus, SSRIs impair serotonin-regulation of reproductive investment
in a planktonic key organism causing inappropriately increased reproduction
with potentially severe ecological impact.