Following peripheral axotomy, long-lasting changes in the expression of neuropeptides and their receptors in primary sensory neurons are observed. These changes involve the downregulation of the excitatory peptides substance P and calcitonin gene-related peptide and the upregulation of the inhibitory peptides neuropeptide tyrosine and galanin, resulting in a reduction of transmission in the dorsal horn. The changes observed are thought to represent adaptive responses to limit the consequences of peripheral nerve damage to the organism as a whole and to promote survival and recovery of the individual neuron.

Plasticity describes a number of different phenomena. In this article it is used to reflect dramatic changes in the expression of peptides, peptide receptors and their mRNAs in primary sensory neurons after a peripheral nerve lesion, leading virtually to a new phenotype. Such changes in gene expression are not unique to primary sensory neurons. For example, at the spinal level, it is well known that axotomy induces changes in peptide levels in motoneurons 1 and that peripheral inflammation causes a marked upregulation of peptides in interneurons in the dorsal horn,