Plasticity of spinal nicotinic acetylcholine receptors following spinal nerve ligation.

The nicotinic cholinergic system is known to be important in the processing of nociceptive information. In the spinal cord, nicotinic receptors are expressed on primary afferent terminals, inhibitory interneurons and descending noradrenergic and serotoninergic fibers. Following peripheral nerve injury, the expression of numerous receptors involved in nociceptive processing is altered in the superficial dorsal horn of the spinal cord. However, the expression of nicotinic acetylcholine receptor subunits in the lumbar spinal cord following peripheral nerve injury has not been investigated. We examined the expression of the alpha3, alpha4, alpha5, alpha7, beta2, beta3 and beta4 nicotinic subunits in the spinal cord of normal and spinal nerve ligated rats using immunocytochemistry. Two nicotinic subunits were found to have an increased expression following spinal nerve ligation. The number of cells expressing the alpha3 subunit in the dorsal horn increased bilaterally following spinal nerve injury. Also, the number of alpha5 immunoreactive fibers increased significantly ipsilateral to ligation. The expression of the alpha4, alpha7, beta2, beta3 and beta4 subunits was unchanged. We propose that the increased expression of the alpha3 and alpha5 nicotinic subunits may contribute to the mechanical hypersensitivity observed following spinal nerve ligation.