ABSTRACT
Primary sensory neurons with cell bodies located in the dorsal root ganglia (DRG), trigeminal and vagal (nodose and jugular) ganglia consist of an heterogeneous neuronal population. A subgroup of these neurons is characterized by the expression of neuropeptides, including calcitonin gene-related peptide (CGRP) and the tachykinins, substance P (SP) and neurokinin A (NKA). Neurons expressing neuropeptides have small, dark cell bodies with unmyelinated (C) or thinly myelinated (A-δ) fibres. These neurons play important roles in the central transmission of painful stimuli and in inflammation of peripheral tissues (Figure 10.1). Thermal, chemical and high-threshold mechanical stimulation of peripheral tissues generates action potentials which are transmitted centrally where they induce the release of neuropeptides within the central nervous system, resulting in the central transmission of nociceptive signals (Otsuka and Yoshioka, 1993). These same stimuli also cause inflammation of peripheral tissues. Antidromic propagation of action potentials can release sensory neuropeptides from peripheral endings of these neurons. The local release of CGRP, SP and NKA from endings of primary sensory neurons in peripheral tissues initiates a variety of responses, collectively referred to as ‘neurogenic inflammation’ (Geppetti and Holzer, 1996). Neurogenic inflammation consists of a series of stereotypic responses, mainly at the vascular level, that include arteriolar vasodilatation, extravasation of plasma proteins from gaps between endothelial cells of post-capillary venules, and adhesion of leukocytes to the vascular endothelium. Additional tissuesspecific components of neurogenic inflammation include various non-adrenergic non-cholinergic (NANC) motor effects, such as the atropine-resistant bronchoconstriction of the guinea pig airways, the contraction and relaxation of rodent urinary bladder, and the miotic response in rodent, rabbit and pig iris smooth muscle (Holzer, 1988; Maggi et al., 1991).
