Plasticity of cutaneous primary afferent projections to the spinal dorsal horn

Reorganization of the somatotopic map in the spinal dorsal horn may be elicited by a variety of deafferenting lesions, including transection of peripheral nerves or dorsal roots, or the application of neurotoxins. While such lesions give rise to a variety of neurochemical and morphological changes in the dorsal horn, collateral sprouting of intact primary afferents appears to be minimal. Recently, intraaxonal injection of neurobiotin has allowed visualization of the entire spinal arborization of single A beta primary afferent fibers in animals where the somatotopy of the relevant region of dorsal horn has also been mapped. In contrast to the somatotopic precision of the terminal fields of peripheral nerves suggested by transganglionic tracing, these studies have shown that afferents make connections many millimeters rostral and caudal to the region where their receptive field is represented in the somatotopic map. Intracellular recording from dorsal horn neurons has further shown that these long-ranging projections make functional, but weak, synaptic connections. Thus the functional somatotopic reorganization that follows nerve lesions in mature animals might be explained simply by an increased synaptic efficacy of these existing projections. In contrast to the negligible sprouting of intact A beta primary afferents, those undergoing axonal regeneration exhibit dense collateral sprouting into deafferented regions of the dorsal horn, particularly the superficial laminae, where the terminal arbors of many small (A delta and C) nociceptive afferent fibres degenerate following peripheral nerve lesions. The inappropriate connections made by these collateral sprouts may partly underlie the painful sequelae of nerve injury in man.