This light and electron microscopic study sought to localize spinal cord interneurons that contribute to the normal and abnormal physiological regulation of spinal sympathetic preganglionic function. Sympathetic preganglionic neurons in caudal C8 through T4 of rat spinal cord were retrogradely labeled with wheat germ agglutinin (WGA) and/or cholera beta subunit (CT beta) following injections into the superior cervical ganglion (SCG). With two exceptions, the observed locations of retrogradely WGA- and CT beta-labeled sympathetic preganglionic neurons were as expected from previous studies. The exceptions were restricted populations of cells in caudal C8 and rostral T1 spinal segments. These neurons were classified as ventrolateral (vlSPN) and ventromedial (vmSPN) sympathetic preganglionic neurons; their somata and dendrites encircled dorsolateral lamina IX motoneurons. Only WGA was transported transneuronally following the retrograde labeling of sympathetic preganglionic neurons. Transneuronally WGA-labeled spinal interneurons were located principally in the reticulated division of lamina V and dorsolateral lamina VII. A strict segmental organization was observed. All transneuronally labeled interneurons were ipsilateral to, and coextensive with, retrogradely WGA-labeled sympathetic preganglionic neurons. Electron microscopic observations suggested that retrograde transsynaptic passage of WGA occurred within the sympathetic preganglionic neuropil and showed further that similar classes of organelles were WGA immunoreactive in retrogradely labeled sympathetic preganglionic neurons and in transneuronally labeled lamina V and lamina VII neurons: 1) cisternae and vesicles at the trans face of the Golgi apparatus, 2) large endosomes/dense bodies, and 3) multivesicular bodies. The data are consistent with two hypotheses: 1) Somatic and visceral primary afferent inputs to thoracic spinal cord modify segmental sympathetic preganglionic function through activation of a disynaptic pathway involving lamina V and/or lamina VII interneurons, and 2) long-loop propriospinal pathways access sympathetic preganglionic neurons through symmetrical, segmental interneuronal circuitry.

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Tetanus toxin (TeTx) causes sympathetic hyperactivity, a major cause of mortality in generalized tetanus, apparently by obstructing the inhibition of sympathetic preganglionic neurons (SPNs). Neuroanatomic tracing and immunohistochemistry were used to investigate whether axon terminals in the intermediolateral cell column (IML) that synapse on SPNs and use the inhibitory neurotransmitter γ‐aminobutyric acid (GABA) may be infected transsynaptically with TeTx. The binding fragment of TeTx (TTC; an atoxic surrogate of TeTx) and the cholera toxin B subunit (CTB; a retrograde tracer) were injected into the rat superior cervical ganglion and, over 16–48 hours, were transported to the ipsilateral IML in the caudal half of the last cervical and first three thoracic spinal cord segments. With light microscopy, diffuse CTB immunolabeling extended throughout SPN perikarya and dendrites. Punctate TTC and GABA immunolabeling were accumulated densely in the neuropil between and surrounding SPN processes. With electron microscopy, 54% of the axon terminals in the IML (n = 1,337 terminals) were TTC immunolabeled (TTC+), and 25% contained putative neurotransmitter levels of GABA immunolabeling (GABA+). On average, GABA+ terminals had a 76% chance of also being TTC+ and a 62% greater chance of being TTC+ than GABA− terminals (P < 0.000001). Axon terminals were just as likely to be TTC+ and/or GABA+ regardless of whether the dendrites they synapsed on were large (>1 μM) or small in cross‐sectional area or were labeled retrogradely. Sympathetic hyperactivity in tetanus may involve 1) retrograde and transsynaptic transport of TeTx by SPNs and 2) at least in part, an infection of GABAergic terminals in the IML. J. Comp. Neurol. 419:471–484, 2000. © 2000 Wiley‐Liss, Inc.