Mast cell-nerve interactions. Inflammatory mediators may modulate sensory nerve endings through the activation of receptors on nerve terminals. Neuropeptides can stimulate mast cells via a receptor-dependent and a receptor-independent mechanism. Under inflammatory-like conditions, receptor expression on nerve endings and mast cells can be up-regulated. CGRP = calcitonin gene-related peptide; H = histamine; 5HT2A = serotonin 2a; NGF = nerve growth factor; NK-1 = neurokinin 1; PAR = protease-activated receptor; TNFR = tumour necrosis factor receptor; trk = neurotrophin tyrosine kinase receptor.