Tresguerres Martin, Hamilton Trevor J
Marine Biology Research Division, Scripps Institution of Oceanography, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA
Department of Psychology, MacEwan University, Edmonton, Alberta, Canada T5J 4S2
J Exp Biol. 2017 Jun 15;220(Pt 12):2136-2148. doi: 10.1242/jeb.144113.
Experimental exposure to ocean and freshwater acidification affects the behaviour of multiple aquatic organisms in laboratory tests. One proposed cause involves an imbalance in plasma chloride and bicarbonate ion concentrations as a result of acid-base regulation, causing the reversal of ionic fluxes through GABA receptors, which leads to altered neuronal function. This model is exclusively based on differential effects of the GABA receptor antagonist gabazine on control animals and those exposed to elevated CO However, direct measurements of actual chloride and bicarbonate concentrations in neurons and their extracellular fluids and of GABA receptor properties in aquatic organisms are largely lacking. Similarly, very little is known about potential compensatory mechanisms, and about alternative mechanisms that might lead to ocean acidification-induced behavioural changes. This article reviews the current knowledge on acid-base physiology, neurobiology, pharmacology and behaviour in relation to marine CO-induced acidification, and identifies important topics for future research that will help us to understand the potential effects of predicted levels of aquatic acidification on organisms.
在实验室测试中,对海洋和淡水酸化的实验性暴露会影响多种水生生物的行为。一种提出的原因涉及酸碱调节导致的血浆氯离子和碳酸氢根离子浓度失衡,从而导致通过GABA受体的离子通量逆转,进而导致神经元功能改变。该模型完全基于GABA受体拮抗剂gabazine对对照动物和暴露于高浓度二氧化碳环境下的动物的不同影响。然而,在很大程度上缺乏对神经元及其细胞外液中实际氯离子和碳酸氢根浓度以及水生生物中GABA受体特性的直接测量。同样,对于潜在的补偿机制以及可能导致海洋酸化引起行为变化的替代机制知之甚少。本文综述了当前关于与海洋二氧化碳诱导的酸化相关的酸碱生理学、神经生物学、药理学和行为的知识,并确定了未来研究的重要课题,这些课题将有助于我们理解预测的水生酸化水平对生物的潜在影响。