Neuroepithelial cells (NEC) are thought to be neuron-like chemoreceptor cells because they rely on membrane potential changes for the release of neurotransmitters and signal transmission onto nearby cells.  Once NEC of the zebrafish gills come in contact with either environmental or aortic hypoxia, an outward K  "leak" channel is inhibited.  It remains unclear how these K channels are inhibited by a shortage of oxygen because there are yet to be any known direct binding sites for "a lack of oxygen", only whole cell and ion channel responses to hypoxia.  K  "leak" channels are two-pore-domain ion channels that are open at the resting membrane potential of the cell and play a major role in setting the equilibrium resting membrane potential of the cell.  Once this "leak" channel is closed, the K is no longer able to freely flow out of the cell, and the membrane potential of the NEC increases; the cell becomes depolarized.  This depolarization causes voltage-gated Ca channels to open, and for extracellular Ca to flow down its concentration gradient into the cell causing the intracellular Ca concentration to greatly increase.  Once the Ca is inside the cell, it binds to the vesicle release machinery and facilitates binding of the t-snare complex on the vesicle to the s-snare complex on the NEC cell membrane which initiates the release of neurotransmitters into the synaptic cleft.