Once an irritating particle enters the trachea and stimulates a receptor a series of events take place. The resting membrane potential of a sensory neuron (usually maintained around -70mV) brought about by the sodium potassium pump, is disrupted due to the slight depolarisation (to around -30mV) of the membrane by the detected stimulus. This causes the sodium voltage gated channels to open, allowing the sodium ions to enter the cell down their concentration and electrical gradients, causing depolarisation of the nerve cell membrane. When a membrane potential of +40mV is reached the sodium voltage gated channels close while the potassium voltage gated channels open. This allows the potassium ions to rapidly leave the cell down their concentration and electrical gradients, resulting in repolarisation. A larger amount of potassium ions leaves the cell than is required to return the resting membrane potential, overshooting and bringing about hyperpolarisation. This allows the action potential to be propagated in one direction towards the brain and later to the effector muscle or gland. Propagation occurs via the axon's nodes of Ranvier of the sensory nerve cell by saltatory conduction until the action potential reaches the pre-synaptic cell membrane. When this area depolarises it causes voltage gated calcium channels to open, and an influx of calcium ions to the cell. This then results in neurotransmitter containing vesicles to migrate towards the pre-synaptic membrane and fuse with it. Exocytosis allows the neurotransmitter to be released into the synaptic cleft where it diffuses across the synapse and binds with the specific receptors on the post synaptic membrane. If enough chemicals bind with the post synaptic membrane, sodium gated channels open and a new action potential is produced and propagated further down the next nerve cell, towards the medulla oblongata of the brain.