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Experiments show that GABAA receptors located on an axon can affect synaptic transmission, presumably through modulation of calcium influx on a presynaptic terminal which determines release of mediator. In this paper, a mathematical model that describes the shunting effect of these receptors on the presynaptic calcium influx is proposed. Simulations show that the effect of GABAA channels depends on their location and reversal potential that is determined by the concentration of chloride accumulated inside the axon. The synaptic channels located in the center of axon cannot stop the propagation of action potential thus not affecting the calcium influx, regardless of the value of the reversal potential. If the receptors are located at the end of the axon, they can influence on the mediator release by means of either the inactivation of calcium channels located on the terminal or the decrease of action potential amplitude, depending on the inactivation thresholds of calcium and sodium channels. In the both cases, the effect is noticeable only for depolarized GABAA reversal potential, i.e. in the conditions of chloride accumulation. Overall, the simulations clarify possible role of GABAA receptors and chloride accumulation on synaptic transmission.