Spinal sympathetic interneurons: their identification and roles after spinal cord injury.
Primary afferent neurons rarely, if ever, synapse on the sympathetic preganglionic neurons that regulate the cardiovascular system, nor do sympathetic preganglionic neurons normally exhibit spontaneous activity in the absence of excitatory inputs. Therefore, after serious spinal cord injury "spinal sympathetic interneurons" provide the sole excitatory and inhibitory inputs to sympathetic preganglionic neurons. Few studies have addressed the anatomy and physiology of spinal sympathetic interneurons, to a great extent because they are difficult to identify. Therefore, this chapter begins with descriptions of both neurophysiological and neuroanatomical criteria for identifying spinal sympathetic interneurons, and it discusses the advantages and disadvantages of each. Spinal sympathetic interneurons also have been little studied because their importance in intact animals has been unknown, whereas the roles of direct projections from the brain to sympathetic preganglionic neurons are better known. This chapter presents evidence that spinal sympathetic interneurons play only a minor role in sympathetic regulation when the spinal cord is intact. However, they play an important role after spinal cord injury, both in generating ongoing activity in sympathetic nerves and in mediating segmental and intersegmental sympathetic reflexes. The spinal sympathetic interneurons that most directly influence the activity of sympathetic preganglionic neurons after spinal cord injury are located close to their associated sympathetic preganglionic neurons, and the inputs from distant segments that mediate multisegmental reflexes are relayed to sympathetic preganglionic neurons multisynaptically via spinal sympathetic interneurons. Finally, spinal sympathetic interneurons are more likely to be excited and less likely to be inhibited by both noxious and innocuous somatic stimuli after chronic spinal transection. The onset of this hyperexcitability corresponds to morphological changes in both sympathetic preganglionic neurons and primary afferents, and it may reflect the pathophysiological processes that lead to autonomic dysreflexia and the hypertensive crises that may occur with it in people after chronic spinal injury.
Schramm
Lawrence P
LP
Department of Biomedical Engineering and Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. LSCHRAMM@bme.jhu.edu
D000818:Animals; D004594:Electrophysiology; D005728:Ganglia, Sympathetic / Q000166:cytology* / Q000473:pathology; D006801:Humans; D007395:Interneurons / Q000166:cytology / Q000378:metabolism*; D013116:Spinal Cord / Q000166:cytology* / Q000378:metabolism; D013119:Spinal Cord Injuries / Q000473:pathology / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000033:anatomy & histology / Q000502:physiology; D013569:Synapses / Q000378:metabolism; D014110:Touch / Q000502:physiology