[4][5][6] Therefore, the olfactory nerve works to transduce sensory stimuli in the form of odorants and encode them into electrical signals, which are relayed to higher-order centers through synaptic transmission.

[4] An individual ORN contains several microvilli, olfactory cilia, which protrude from a knoblike structure at the apical surface involved in dendritic processes.

[4][5] At the axon hillock, voltage-gated Na+ channels open and generate an action potential that is transmitted to the olfactory bulb.

[4][5] After transmission, the ORN membrane is repolarized by calcium/calmodulin kinase II-mediated mechanisms that work to extrude Ca2+ and transport Na+ via an Na+/Ca2+ exchanger, diminish cAMP levels by activating phosphodiesterases, and restore heterotrimeric Golf.

[4] ORN axons are responsible for relaying odorant information to CNS through action potentials.

[4][5][6] The ORN axons of each glomerulus synapse with apical dendrites of mitral cells, the primary projection neurons of the olfactory bulb, which create and send action potentials further into the CNS.

[4] In the nasal passages, inhaled odorant molecules interact with receptor proteins on localized neuronal cilia of ORNs.

[4] Damage to this nerve leads to impairment or total loss of the sense of smell (anosmia).

[2] Lesions to the olfactory nerve can occur because of "blunt trauma", such as coup-contrecoup damage, meningitis, and tumors of the frontal lobe of the brain.

Lesions of the olfactory nerve do not lead to a reduced ability to sense pain from the nasal epithelium.

A decrease in the ability to smell is a normal consequence of human aging, and usually is more pronounced in men than in women.