Deprivation of vibrissae from an early age causes plasticity in S1 barrel cortex. This method of deprivation is most likely to induce plasticity by altering the balance of primary afferent activity from the deprived and spared vibrissae. To study whether or not induction or expression of this type of plasticity might be affected by follicle nerve injury caused by the deprivation technique, three different methods of detecting nerve injury were used: counting axon numbers in the distal follicle nerve, quantifying morphological changes in axons, and measuring neuropeptide expression in the trigeminal ganglion cells. First, nerves innervating follicles chronically deprived of vibrissae from birth had the same number of myelinated and unmyelinated axons as nerves from normally reared animals. Second, axons innervating deprived follicles showed no morphological changes in myelination or mitochondria characteristic of damaged nerves. Third, the corresponding nerve cell bodies in the trigeminal ganglion did not show upregulation of galanin or neuropeptide Y expression. In contrast, animals receiving mild injury of the follicle nerve endings (by cauterization of the follicle) showed profound changes in axonal myelination and mitochondria and increases in neuropeptide expression. These results imply that vibrissae deprivation does not act by inducing injury of the follicular nerve, suggesting that changes in the balance of follicle nerve activity are the cause of cortical plasticity. Consistent with this notion, a fourth experiment demonstrated that trimming the vibrissae induces cortical plasticity comparable to that induced by complete vibrissae removal.