Impaired Learned and Lower Prey Survival Under Elevated CO2 Caused from Neurotransmitter Interference

Ocean acidification is known to have physiology impacts and large ecological consequences on marine species. However, the mechanisms by which these impacts occur are somewhat unknown. Chivers et al. (2013) studied the effect of end of century CO2 concentrations on the ability of larval damselfish to learn to identify predators. The damselfish were exposed to a predator odor coupled with an alarm cue designed to stimulate learning within the fish to learn to avoid that predator. The fish were then exposed the odor a few days later to see if they had successfully learned to identify the predator. Fish were then put in the wild and the survival rate was monitored. The authors found that there was impaired neurotransmitter function within the elevated-CO2 fish. This impaired learning was reversed with gabazine, an antagonist of the GABA-A receptor—a neurotransmitter that manages risk assessment in vertebrates. Overall, elevated CO2 lead to an impairment in learning within the lab setting and also lowered fish survival rates in the wild. With lower survival as a result of impaired learning, there could be negative implications for reef population recruitment as well as changes in species dynamics with near future CO2 concentrations.–Submitted by Jennifer Fields

Chivers, D.P., McCormick, M.I., Nilsson, G.E., Munday, P.L., Watson, S.A., Meekan, M.G., Mitchell, M.D., Corkill, K.C., Ferrari, M.C.O. 2013. Impaired Learning of Predators and Lower Prey Survival Under Elevated CO2: a Consequence of Neurotransmitter Interference. Global Climate Change published ahead of print May 30, 2013,doi:10.1111/gcb.12291

Under ocean acidification conditions, fish have exhibited an inability to learn to sense predators and have experienced decreased survival and recruitment. It has been previously determined that this inability is caused by a dysfunction in the GABA-A neurotransmitter in the fish’s brain. Chivers et al. (2013) wished to examine how widespread GABA-A reception malfunction in the fish brain affects higher cognitive function. To do this, the authors exposed larval damselfish to predicted near-future CO2 levels and conducted two experiments with the addition of gabazine, an antagonist of GABA-A. The first experiment tested whether altered GABA-A function was responsible for the effects of elevated CO2 on learning. The second experiment tested the restoration of the GABA-A receptor by the use of gabazine through monitoring the survival rate of the fish when released into the wild onto patch reefs. Fish were placed in elevated CO2 or control water for four days prior to the experiments with or without the addition of gabazine. For the learning experiment, the fish were exposed to a predator odor coupled with an alarm cue, which is the chemical cue released when fish die. The fish were placed in an experimental tank with food and the predator odor was added. The authors noted if there was a reduction in feeding and activity with the addition of the predator odor. The experiment was conducted on day one and day five after CO2 exposure to see if learning had occurred. For the next experiment, fish that went through the same learning experiment were placed onto patch reefs in the wild and survival rate was monitored for four days.

As predicted by the authors, there was impaired learning within the elevated CO2 fish as a result of diminished neurotransmitter function. Control fish displayed an anti-predator response, classified as reduced activity and feeding, when exposed to the predator odor regardless of the gabazine treatment. Fish in elevated CO2 did not change their behavior when the predator odor was added, suggesting that the prey did not learn to identify the predator. However, the elevated-CO2 fish treated with gabazine prior to the learning experiment responded to the predator after five days of learning, indicating that the presence of gabazine allowed learning to occur. When the fish were put into the wild, elevated CO2 impaired the survival of the fish. However, this survival rate was improved by the addition of gabazine in the treatment, suggesting that the treatment of gabazine reduced the CO2 effect sufficiently enough to allow associative learning through chemical cues to occur.

The results demonstrate that with the proposed end of this century CO2 concentrations, there will be impairment in the ability for damselfish to recognize predators. With the addition of gabazine after five days, the effect of elevated CO2 was diminished and learning ability was restored, suggesting that malfunction in the GABA-A neurotransmitter is the main cause of the behavioral changes with increased CO2 concentrations. The reef ecosystem’s health depends on the ability to recruit juvenile fish, but predators remove up to 60% of new recruits to the reef within the first two days. Under elevated CO2, the rate of mortality increased 2.53 times normal mortality rates. This could create a significant decrease in population recruitment and has the potential to alter the structure of coral reef communities.

Ocean acidification has the potential to change marine community dynamics all over the world. Elevated CO2 will alter the neurology of species directly leading to changes in behavior, learning, and ultimately survival in the wild. Many of these alterations will depend on the ability of species to adapt to increased CO2 concentrations. However, decreased learning and survival in larval fish will certainly change the dynamics of marine communities through decreased population recruitment.


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