Properties of intact and injured sensory neurons with nerve growth factor receptors

The role of nerve growth factor (NGF), a neurotrophic molecule, and its high-affinity receptor in intact and injured adult rat lumbar sensory neurons was examined at a cellular level using quantitative receptor radioautography to localize the NGF high-affinity receptor-positive subpopulation, in conjunction with histochemistry on adjacent sections. The 40-50% of sensory neurons displaying NGF receptors were characterized. Virtually all neurons containing substance P or CGRP were NGF receptor-positive, but not those with somatostatin or thiamine monophosphatase activity. The ability of a neuron to bind NGF with high-affinity correlates positively with growth-associated protein (GAP43) expression but not with neurofilament (NFM) expression. Following injury, sensory neurons atrophy, lose NGF receptors, decrease NFM expression, while GAP43 expression is elevated in all neurons irrespective of their ability to bind NGF. Infusion of NGF for 1 week, at the time of injury or 3 weeks following injury counteracts NGF receptor loss, cell atrophy, and decreased NFM expression, but only in those neurons bearing NGF receptors. GAP43 expression remained high in all neurons despite infusion. NGF's function in normal sensory neurons appears to be modulatory, permitting regulation of intrinsic properties. Injury disrupts this permissive state, which can be restored with exogenous NGF