The nature of dorsal root reflexes (DRRs) and their possible role in peripheral inflammation and the consequent hyperalgesia are reviewed. The history of DRRs and the relationship of DRRs to primary afferent depolarization and presynaptic inhibition in pathways formed by both large and fine afferents are discussed. Emphasis is placed on the mechanisms underlying primary afferent depolarization, including the anatomical arrangement of the synapses involved, how depolarization can result in inhibition by decreasing transmitter release, the role of excitatory amino acids and GABA, the manner in which the equilibrium potential for chloride ions is determined in primary afferent fibers, and forms of presynaptic inhibition that do not utilize GABA(A) receptors. There is then a discussion of neurogenic inflammation, including the role of the release of neuropeptides such as substance P and calcitonin gene-related peptide from sensory nerve endings. Evidence is reviewed that links DRRs to a substantial part of the swelling of the knee joint in acute experimental arthritis and to the flare reaction in the skin following intradermal injection of capsaicin. Possible mechanisms by which the level of DRR activity might be enhanced following inflammation are suggested. The consequences of this increase in DRRs may include exacerbation of hyperalgesia as well as of peripheral inflammation. The conversion of an inhibitory process, presynaptic inhibition, to an excitatory one by DRRs can thus lead to pathological consequences.

No abstract

The substantia gelatinosa of the mammalian spinal cord is generally believed to be a closed system; that is its neurons are thought to project only to the substantia gelatinosa of the same or the contralateral side. Experiments in monkeys, using injections of the marker enzyme horseradish peroxidase, show that at least some neurons of the substantia gelatinosa project to the thalamus and thus belong to the spinothalamic tract. Such neurons include two cell types intrinsic to the gelatinosa, the central cells and the limitrophe cells of Cajal.

In primates, the principal nociceptive pathways ascend in the anterolateral quadrant of the spinal cord. Among these, the spinothalamic tract (s.t.t.) is the best studied. Cells in Rexed's laminae I and V project to the ventro-posterolateral (v.p.l.) thalamic nucleus. Other cells in the same and deeper laminae terminate in the intralaminar complex. Spinothalamic tract cells may be nociceptive-specific or multireceptive. Those ending in v.p.l. have restricted, contralateral receptive fields, whereas those projecting to the intralaminar region often have large, bilateral receptive fields. Spinoreticular tract (s.r.t.) cells are concentrated in laminae VII and VIII and may be nociceptive. It is proposed that the s.t.t. contributes to sensory-discriminative processing of pain and that the s.t.t. and s.r.t. play a role in the motivational-affective components of pain. Alternative nociceptive pathways are the spinocervical and postsynaptic dorsal column tracts.

There are a number of discrete electro-physiological responses which can be recorded from the ventral horn. Those which can be related to anatomically defined structures, or at least to positions within the laminae of Rexed, include the responses of α-motoneurons, γ-motoneurons, α-motor axons, Renshaw cells, type A interneurons, and commissural neurons. Recurrent inhibition is best explained by the excitation of Renshaw cells by recurrent collaterals of motor axons; Renshaw cells in turn inhibit motoneurons. The synaptic transmitter released by the recurrent collaterals is acetylcholine. That released by Renshaw cells may be glycine or a related substance. Recurrent facilitation is best explained by the inhibition by Renshaw cells of inhibitory interneurons. Candidate inhibitory interneurons include type A interneurons, which may mediate group I reciprocal inhibition, and other Renshaw cells. There is no good reason to believe that Renshaw cells are actually the terminals of recurrent collaterals or the dendrites of motoneurons rather than interneurons. However, there is also no convincing evidence that Renshaw cells are necessarily short-axoned cells.