A major catalyst for climate change is the burning of fossil fuels which has caused the fastest increase in atmospheric carbon dioxide (CO2) in recorded history. Seawater surface CO2 concentrations are projected to quadruple compared to pre-industrial levels by the end of the century and increase up to seven-fold by 2300 AD. As many enzymatic reactions require narrow pH milieus for optimal function, marine organisms require a tightly controlled acid-base homeostasis for survival. In fish, exposure to elevated CO2 levels causes hypercapnia (increase of blood plasma CO2 levels) and respiratory acidosis, which requires compensatory changes in their bicarbonate metabolism to stabilize plasma pH. These changes are hypothesized to weaken inhibitory synapses by raising the reversal potential of GABAergic receptors. To allow for synchronized swimming motions, lampreys have evolved a spinal rhythmic pattern generator consisting of an interplay between excitatory and inhibitory synapses that result in phasic activity of motor neurons – with both types of synapses being modulated by presynaptic GABAA receptors. I will perform electrophysiological whole-cell in vitro recordings in ventral root motor neurons from animals adapted to different degrees of hypercapnia to study the effects of CO2 on the resilience of this system on a synapse and circuit level. By performing swimming assays, I will study the effects of hypercapnia on the resulting swimming motions.