The effect of peripheral nerve lesions and of neonatal capsaicin in the rat on primary afferent depolarization

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Abstract
In anesthetized adult rats with intact peripheral nerves, a conditioning orthodromic volley in myelinated afferents produces a prolonged increase in the excitability of the terminals of the afferents which have carried the orthodromic volley and in the terminals of their passive neighbors. This phenomenon, primary afferent depolarization (PAD), is shown by the antidromic stimulation of afferents with a microelectrode in the dorsal horn and by recording the antidromic volley on a cut peripheral nerve. If a peripheral nerve is cut and ligated, the size of the myelinated afferent volley generated by stimulation proximal to the cut and measured on dorsal roots is not affected for 14 days after the cut. The size of the volleys ascending the cord in axons from cord cells remains unaffected. If a peripheral nerve is cut and tested after 7-14 days, it produces a markedly decreased PAD on itself and on its neighbors. If a nerve is crushed rather than cut, it produces a normal PAD on itself and its neighbors after 7-14 days. In animals treated neonatally with capsaicin, there is a severe loss of unmyelinated afferents. Testing the effect of an orthodromic volley in myelinated afferents on the excitability of myelinated afferent central terminals shows that there is a strongly decreased PAD in these animals. PAD is sensitive to peripheral nerve lesions and may be particularly dependent on the integrity of the unmyelinated afferents in spite of the fact that PAD is measured as a phenomenon of myelinated afferents acting on myelinated afferents.