ABSTRACT
INTRODUCTION The conditions of inhaled air activate trigeminal type A and C afferent neurons. Distinct subpopulations of afferent neurons are presumed to have unique combinations of afferent sensor proteins, sodium, and other ion channels. These are involved in neural depolarization and the spread of the action potential throughout the extensively branched nasal ramification of nerve endings, and transmission to the dorsal root ganglion cell bodies and central nervous system. Some of the branched neurons release neurotransmitters locally in the nasal mucosa to generate the axon response of “neurogenic inflammation.” The axon response in human nasal mucosa leads to glandular secretion without any change in vascular processes. This activation-exocytosis loop is a very rapid onset nasal defense mechanism. Depolarization of dorsal root ganglion cells may alter the amount and identity of sensor proteins and neurotransmitters and so alter the functions of these neurons (“neural plasticity”).
