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Current concepts in neuroendocrine disruption
#MMPMID24530523
León-Olea M
; Martyniuk CJ
; Orlando EF
; Ottinger MA
; Rosenfeld C
; Wolstenholme J
; Trudeau VL
Gen Comp Endocrinol
2014[Jul]; 203
(?): 158-173
PMID24530523
show ga
In the last few years, it has become clear that a wide variety of environmental
contaminants have specific effects on neuroendocrine systems in fish, amphibians,
birds and mammals. While it is beyond the scope of this review to provide a
comprehensive examination of all of these neuroendocrine disruptors, we will
focus on select representative examples. Organochlorine pesticides bioaccumulate
in neuroendocrine areas of the brain that directly regulate GnRH neurons, thereby
altering the expression of genes downstream of GnRH signaling. Organochlorine
pesticides can also agonize or antagonize hormone receptors, adversely affecting
crosstalk between neurotransmitter systems. The impacts of polychlorinated
biphenyls are varied and in many cases subtle. This is particularly true for
neuroedocrine and behavioral effects of exposure. These effects impact sexual
differentiation of the hypothalamic-pituitary-gonadal axis, and other
neuroendocrine systems regulating the thyroid, metabolic, and stress axes and
their physiological responses. Weakly estrogenic and anti-androgenic pollutants
such as bisphenol A, phthalates, phytochemicals, and the fungicide vinclozolin
can lead to severe and widespread neuroendocrine disruptions in discrete brain
regions, including the hippocampus, amygdala, and hypothalamus, resulting in
behavioral changes in a wide range of species. Behavioral features that have been
shown to be affected by one or more these chemicals include cognitive deficits,
heightened anxiety or anxiety-like, sociosexual, locomotor, and appetitive
behaviors. Neuroactive pharmaceuticals are now widely detected in aquatic
environments and water supplies through the release of wastewater treatment plant
effluents. The antidepressant fluoxetine is one such pharmaceutical
neuroendocrine disruptor. Fluoxetine is a selective serotonin reuptake inhibitor
that can affect multiple neuroendocrine pathways and behavioral circuits,
including disruptive effects on reproduction and feeding in fish. There is
growing evidence for the association between environmental contaminant exposures
and diseases with strong neuroendocrine components, for example decreased
fecundity, neurodegeneration, and cardiac disease. It is critical to consider the
timing of exposures of neuroendocrine disruptors because embryonic stages of
central nervous system development are exquisitely sensitive to adverse effects.
There is also evidence for epigenetic and transgenerational neuroendocrine
disrupting effects of some pollutants. We must now consider the impacts of
neuroendocrine disruptors on reproduction, development, growth and behaviors, and
the population consequences for evolutionary change in an increasingly
contaminated world. This review examines the evidence to date that various
so-called neuroendocrine disruptors can induce such effects often at
environmentally-relevant concentrations.
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