Exotic asphyxiation: interactions between invasive species and hypoxia.

Non-indigenous species (NIS) and hypoxia (<2 mg O2 l-1 ) can disturb and restructure aquatic communities. Both are heavily influenced by human activities and are intensifying with global change. As these disturbances increase, understanding how they interact to affect native species and systems is essential. To expose patterns, outcomes, and generalizations, we thoroughly reviewed the biological invasion literature and compiled 100 studies that examine the interaction of hypoxia and NIS. We found that 64% of studies showed that NIS are tolerant of hypoxia, and 62% showed that NIS perform better than native species under hypoxia. Only one-quarter of studies examined NIS as creators of hypoxia; thus, NIS are more often considered passengers associated with hypoxia, rather than drivers of it. Paradoxically, the NIS that most commonly create hypoxia are primary producers. Taxa like molluscs are typically more hypoxia tolerant than mobile taxa like fish and crustaceans. Most studies examine individual-level or localized responses to hypoxia; however, the most extensive impacts occur when hypoxia associated with NIS affects communities and ecosystems. We discuss how these influences of hypoxia at higher levels of organization better inform net outcomes of the biological invasion process, i.e. establishment, spread, and impact, and are thus most useful to management. Our review identifies wide variation in the way in which the interaction between hypoxia and NIS is studied in the literature, and suggests ways to address the number of variables that affect their interaction and refine insight gleaned from future studies. We also identify a clear need for resource management to consider the interactive effects of these two global stressors which are almost exclusively managed independently.

Excitatory actions of GABA mediate severe-hypoxia-induced depression of neuronal activity in the pond snail (Lymnaea stagnalis).

To characterize the effect of severe hypoxia on neuronal activity, long-term intracellular recordings were made from neurones in the isolated central ring ganglia of Lymnaea stagnalis. When a neurone at rest in normoxia was subjected to severe hypoxia, action potential firing frequency decreased by 38% (from 2.4-1.5 spikes s(-1)), and the resting membrane potential hyperpolarized from -70.3 to -75.1 mV. Blocking GABA(A) receptor-mediated synaptic transmission with the antagonist bicuculline methiodide (100 micromol l(-1)) decreased neuronal activity by 36%, and prevented any further changes in response to severe hypoxia, indicating that GABAergic neurotransmission mediates the severe hypoxia-induced decrease in neuronal activity. Puffing 100 micromol l(-1) GABA onto the cell body produced an excitatory response characterized by a transient increase in action potential (AP) firing, which was significantly decreased in severe hypoxia. Perturbing intracellular chloride concentrations with the Na+/K+/Cl- (NKCC1) cotransporter antagonist bumetanide (100 micromol l(-1)) decreased AP firing by 40%, consistent with GABA being an excitatory neurotransmitter in the adult Lymnaea CNS. Taken together, these studies indicate that severe hypoxia reduces the activity of NKCC1, leading to a reduction in excitatory GABAergic transmission, which results in a hyperpolarization of the resting membrane potential (Vm) and as a result decreased AP frequency.