Zélia Velez

A possible explanation for acidification-induced changes in fish behaviour is that acidification interferes with neurogenesis and modifies the plasticity of neuronal circuitry in the brain. We tested the effects on the olfactory system and brain of gilthead seabream (Sparus aurata) to 4 weeks' exposure to ocean acidification (OA). Olfactory epithelium (OE) morphology changed shortly after OA exposure and persisted over the 4 weeks. Expression of genes related to olfactory transduction, neuronal excitability, synaptic plasticity, GABAergic innervation, and cell proliferation were unchanged in the OE and olfactory bulb (OB) after 4 weeks' exposure. Short-term changes in the ionic content of plasma and extradural fluid (EDF) returned to control levels after 4 weeks' exposure, except for [Cl−], which remained elevated. This suggests that, in general, there is an early physiological response to OA and by 4 weeks a new homeostatic status is achieved. However, expression of genes involved in proliferation, differentiation and survival of undifferentiated neurons were modified in the brain. In the same brain areas, expression of thyroid hormone signalling genes was altered suggesting modifications in the thyroid-system may be linked to the changes in neuroplasticity and neurogenesis. Overall, the results of the current study are consistent with and effect of OA on neuroplasticity.

Exposure to high PCO2/low pH seawater induces behavioural alterations in fish; a possible explanation for this is a reversal of Cl−/HCO3− currents through GABAA receptors (the GABAA receptor theory). However, the main evidence for this is that gabazine, a GABAA receptor antagonist, reverses these effects when applied to the water, assuming that exposure to systems other than the CNS would be without effect. Here, we show the expression of both metabotropic and ionotropic GABA receptors, and the presence of GABAA receptor protein, in the olfactory epithelium of gilthead seabream. Furthermore, exposure of the olfactory epithelium to muscimol (a specific GABAA receptor agonist) increases or decreases the apparent olfactory sensitivity to some odorants. Thus, although the exact function of GABAA receptors in the olfactory epithelium is not yet clear, this may complicate the interpretation of studies wherein water-borne gabazine is used to reverse the effects of high CO2 levels on olfactory-driven behaviour in fish.