Catecholaminergic primary sensory neurons: autonomic targets and mechanisms of transmitter regulation

Contrary to traditional teaching, mammalian primary sensory neurons may express catecholaminergic (CA) neurotransmitter characteristics in vivo. Sensory neurons in the nodose, petrosal, and dorsal root ganglia of rats express tyrosine hydroxylase, the rate-limiting enzyme in CA biosynthesis, and formaldehyde-induced CA fluorescence, in addition to other CA traits. These findings suggest that catecholamines may function as sensory as well as autonomic motor (e.g., sympathetic) neurotransmitters. Most CA cells in the petrosal ganglion project peripherally to the carotid body, which indicates a striking correlation between CA expression in sensory neurons and the pattern of sensory innervation. Inasmuch as petrosal ganglion afferents make synaptic contact with chemoreceptive glomus cells in the carotid body, it is likely that CA sensory neurons in the ganglion transmit chemoreceptor information to the brain stem. Comparison with sympathetic neurons indicates that some mechanisms of CA regulation, such as altered activity of tyrosine hydroxylase in response to depolarizing stimuli, are shared among sensory and traditional CA populations. Other mechanisms, including trophic regulation, appear to be distinct. Therefore, despite expression of common phenotypic traits, CA expression in diverse populations of peripheral neurons is not necessarily associated with a common repertoire of regulatory mechanisms.