Separation of the medullo-spinal descending pathway for somatic and autonomic outflow in the cat

The present study investigated differences between vestibulo-somatic and vestibulo-sympathetic reflexes, along with differences between somatic and autonomic spino-bulbo-spinal (SBS) reflexes in chloralose-urethane anesthetized cats. Electrical stimulation was applied to the vestibular nerve (V) for a duration of 0.3 ms. The potential responses in the sympathetic renal nerve (RN) and somatic lumbar nerve were recorded simultaneously. Responses were recorded for a variety of conditioning stimulus to testing stimulus intervals, and the results were plotted to form a recovery curve. The recovery curve for the test response from the somatic nerve was very different from that of the sympathetic nerve. Following transection of the lateral part of the thoracic cord, in the case of the sympathetic renal nerve, recorded responses were still present on vestibular and lumbar nerve stimulation, whereas in the case of the vestibulo-somatic and somatic SBS reflexes, the reflex response had disappeared after transection. These findings suggest that sympathetic and somatic reactions as a result of vestibular stimulation have different descending pathways in the spinal cord, and that their physiological characteristics are different.     

Supraspinal regulation of spinal reflex discharge into cardiac sympathetic nerves

(1) In chloralose anaesthetized cats, reflex responses were recorded in inferior cardiac nerves following stimulation of intercostal nerves and hind limb afferent nerves. (2) In 80% of cats, a long latency reflex response alone was recorded, whereas, in the others, a short and long latency response was present to intercostal nerve stimulation. (3) In cats displaying only a long latency somatocardiac reflex response, damage to the ventral quadrant of the ipsilateral cervical spinal cord, through which runs a bulbospinal inhibitory pathway, resulted in the appearance of shorter latency reflexes to intercostal nerve stimulation. Lesions elsewhere in the cervical cord did not do this. (4) The characteristics of the early responses indicated that they were somatosympathetic reflexes and not dorsal root reflexes. (5) The early reflexes remained and the late reflex disappeared on subsequent complete transection of the spinal cord. The early reflexes were therefore spinal reflexes, and suppressed in the animal with cord intact. (6) Lesions at C4, which included a contralateral hemisection and a section of dorsal columns extending into the dorsal part of the lateral funiculus, abolished the inhibition of a sympathetic reflex that followed stimulation of some somatic afferent nerve fibres. These sections did not release the spinal reflex. Therefore, this reflex inhibition was not responsible for the suppression of the spinal somatosympathetic reflex. (7) The descending inhibitory influence on the segmental reflex pathway was not antagonized by strychnine, bicuculline or picrotoxin. (8) The possibility is discussed that the spinal reflex pathway into cardiac sympathetic nerves is tonically inhibited by a bulbospinal pathway originating from the classical depressor region of the ventromedial reticular formation.     

Endogenous galanin is required for the full expression of central sensitization following peripheral nerve injury.

The neuropeptide galanin is known to be involved in nociceptive sensory processing in the spinal cord. We have attempted to better characterise the function of endogenous galanin in nociceptive signalling by examining a mouse strain carrying a loss of function mutation in the galanin gene (gal-/-). Galanin expression is significantly up-regulated following damage to a peripheral nerve. To address what effect this up-regulation has on spinal cord excitability we have examined wild type (gal+/+) and gal-/- mice 3 days after complete transection of the sciatic nerve using an electrophysiological paradigm, the flexor withdrawal reflex. We demonstrate that the up-regulation of galanin has no direct effect on basal spinal excitability after nerve injury. However, galanin is shown to be a crucial neuromodulator involved in the development of the central sensitization as both windup and the facilitation of spinal reflexes following conditioning stimulation are significantly impaired in gal-/- mice following peripheral nerve injury.     

Nontraumatic spinal intramedullary hemorrhage in an infant

After an uncomplicated pregnancy and delivery, this female child suddenly became quadriplegic on the fifth day of life. She gradually regained movement in her upper extremities. At 2 months of age, she exhibited paraplegia with exaggerated deep tendon reflexes in the lower extremities. Babinski reflex was present bilaterally and sensory disturbances below the trunk were suspected. Somatosensory evoked potentials after median and ulnar nerve stimulation revealed preserved conduction from the upper extremities through the cervical spinal cord to the cortex. Somatosensory evoked potentials after posterior tibial nerve stimulation suggested disturbed conduction in the upper thoracic spinal cord. Magnetic resonance imaging disclosed a hypodense area in the thoracic cord between T1 and T4 on both the T1-weighted and gradient echo images consonant with an old hematoma cavity. Digital subtraction angiography failed to demonstrate any vascular malformation.     

Electrical stimulation combined with exercise increase axonal regeneration after peripheral nerve injury

Although injured peripheral axons are able to regenerate, functional recovery is usually poor after nerve transection. In this study we aim to elucidate the role of neuronal activity, induced by nerve electrical stimulation and by exercise, in promoting axonal regeneration and modulating plasticity in the spinal cord after nerve injury. Four groups of adult rats were subjected to sciatic nerve transection and suture repair. Two groups received electrical stimulation (3 V, 0.1 ms at 20 Hz) for 1 h, immediately after injury (ESa) or during 4 weeks (1 h daily; ESc). A third group (ES+TR) received 1 h electrical stimulation and was submitted to treadmill running during 4 weeks (5 m/min, 2 h daily). A fourth group performed only exercise (TR), whereas an untreated group served as control (C). Nerve conduction, H reflex and algesimetry tests were performed at 1, 3, 5, 7 and 9 weeks after surgery, to assess muscle reinnervation and changes in excitability of spinal cord circuitry. Histological analysis was made at the end of the follow-up. Groups that received acute ES and/or were forced to exercise in the treadmill showed higher levels of muscle reinnervation and increased numbers of regenerated myelinated axons when compared to control animals or animals that received chronic ES. Combining ESa with treadmill training significantly improved muscle reinnervation during the initial phase. The facilitation of the monosynaptic H reflex in the injured limb was reduced in all treated groups, suggesting that the maintenance of activity helps to prevent the development of hyperreflexia.     

The Inhibitory Effects of Pudendal Nerve Stimulation on Bladder Overactivity in Spinal Cord Injury Dogs: Is Early Stimulation Necessary?

Objective: To determine the inhibitory effects of pudendal nerve stimulation (5 Hz) on bladder overactivity at early and late stages of spinal cord injury in dogs. Materials and Methods: The study was performed in eight dogs with chronic spinal cord transection at the T9‐T10 level. Group 1 (four dogs) underwent electrical stimulation of pudendal nerve one month after spinal cord transection. Group 2 (four dogs) underwent stimulation six months after spinal cord transection. The bladders were removed for histological examination of fibrosis after the stimulation. Results: The bladder capacity and the compliance were significantly increased (p < 0.05) by pudendal nerve stimulation in group 1, but not in group 2. The nonvoiding contractions were inhibited in both groups by electrical stimulation. Collagen fiber was increased, while elastic fiber was significantly decreased (p < 0.05) in group 2 when compared with group 1. Conclusion: Pudendal nerve stimulation can increase the bladder capacity and compliance only during the early period before the bladder wall becomes fibrosit and can inhibit the nonvoiding contraction during two stages.     

Bladder emptying by intermittent electrical stimulation of the pudendal nerve

Persons with a suprasacral spinal cord injury cannot empty their bladder voluntarily. Bladder emptying can be restored by intermittent electrical stimulation of the sacral nerve roots (SR) to cause bladder contraction. However, this therapy requires sensory nerve transection to prevent dyssynergic contraction of the external urethral sphincter (EUS). Stimulation of the compound pudendal nerve trunk (PN) activates spinal micturition circuitry, leading to a reflex bladder contraction without a reflex EUS contraction. The present study determined if PN stimulation could produce bladder emptying without nerve transection in cats anesthetized with alpha-chloralose. With all nerves intact, intermittent PN stimulation emptied the bladder (64 +/- 14% of initial volume, n = 37 across six cats) more effectively than either distention-evoked micturition (40 +/- 19%, p < 0.001, n = 27 across six cats) or bilateral intermittent SR stimulation (25 +/- 23%, p < 0.005, n = 4 across two cats). After bilateral transection of the nerves innervating the urethral sphincter, intermittent SR stimulation voided 79 +/- 17% (n = 12 across three cats), comparable to clinical results obtained with SR stimulation. Voiding via intermittent PN stimulation did not increase after neurotomy (p > 0.10), indicating that PN stimulation was not limited by bladder-sphincter dyssynergia. Intermittent PN stimulation holds promise for restoring bladder emptying following spinal injury without requiring nerve transection.     

Artificial autonomic reflexes: using functional electrical stimulation to mimic bladder reflexes after injury or disease

Autonomic reflexes controlling bladder storage (continence) and emptying (micturition) involve spinal and supraspinal nerve pathways, with complex mechanisms coordinating smooth muscle activity of the lower urinary tract with voluntary muscle activity of the external urethral sphincter (EUS). These reflexes can be severely disrupted by various diseases and by neurotrauma, particularly spinal cord injury (SCI). Functional electrical stimulation (FES) refers to a group of techniques that involve application of low levels of electrical current to artificially induce or modify nerve activation or muscle contraction, in order to restore function, improve health or rectify physiological dysfunction. Various types of FES have been developed specifically for improving bladder function and while successful for many urological patients, still require substantial refinement for use after spinal cord injury. Improved knowledge of the neural circuitry and physiology of human bladder reflexes, and the mechanisms by which various types of FES alter spinal outflow, is urgently required. Following spinal cord injury, physical and chemical changes occur within peripheral, spinal and supraspinal components of bladder reflex circuitry. Better understanding of this plasticity may determine the most suitable methods of FES at particular times after injury, or may lead to new FES approaches that exploit this remodeling or perhaps even influence the plasticity. Advances in studies of the neuroanatomy, neurophysiology and plasticity of lumbosacral nerve circuits will provide many further opportunities to improve FES approaches, and will provide "artificial autonomic reflexes" that much more closely resemble the original, healthy neuronal regulatory mechanisms.     

Effects of exercise and fetal spinal cord implants on the H-reflex in chronically spinalized adult rats

This study investigated the modulation of hindlimb reflex excitability after transection of the spinal cord in adult rats. After transection, the H-reflex exhibited decreased depression at high stimulation frequencies compared to intact animals. Groups of animals which received a spinal cord transection followed by either an exercise regimen for the hindlimbs or a fetal spinal cord implant, showed high stimulation frequency depression similar to controls. This suggests that each of these palliative strategies helped to ‘normalize’ the excitability of specific spinal reflexes.     

Effects of sacrocaudal spinal cord transection and transplantation of fetal spinal tissue on withdrawal reflexes of the tail

Reflex responses to electrocutaneous stimulation of the tail were characterized in awake cats, before and after transection of the spinal cord at sacrocaudal levels S3-Ca1. Consistent with effects of spinal transection at higher levels, postoperative cutaneous reflexes were initially depressed, and the tail was flaccid. Recovery ensued over the course of 70-90 days after sacrocaudal transection. Preoperative and chronic postlesion reflexes elicited by electrocutaneous stimulation were graded in amplitude as a function of stimulus intensity. Chronic postlesion testing of electrocutaneous reflexes revealed greater than normal peak amplitudes, peak latencies, total amplitudes (power), and durations, particularly for higher stimulus intensities. Thus, sacrocaudal transection produced effects representative of the spastic syndrome. In contrast, exaggerated reflex responsivity did not develop for a group of cats that received transplants of fetal spinal cord tissue within sacrocaudal transection cavities at the time of injury, in conjunction with long-term immunosuppression by cyclosporine. We conclude that gray matter replacement and potential neuroprotective actions of the grafts and/or immunosuppression prevent development of the spastic syndrome. This argues that the spastic syndrome does not result entirely from interruption of long spinal pathways.     

Effect of electrical stimulation on neural regeneration via the p38-RhoA and ERK1/2-Bcl-2 pathways in spinal cord-injured rats

Although electrical stimulation is therapeutically applied for neural regeneration in patients, it remains unclear how electrical stimulation exerts its effects at the molecular level on spinal cord injury(SCI). To identify the signaling pathway involved in electrical stimulation improving the function of injured spinal cord, 21 female Sprague-Dawley rats were randomly assigned to three groups: control(no surgical intervention, n = 6), SCI(SCI only, n = 5), and electrical simulation(ES; SCI induction followed by ES treatment, n = 10). A complete spinal cord transection was performed at the 10~(th) thoracic level. Electrical stimulation of the injured spinal cord region was applied for 4 hours per day for 7 days. On days 2 and 7 post SCI, the Touch-Test Sensory Evaluators and the Basso-Beattie-Bresnahan locomotor scale were used to evaluate rat sensory and motor function. Somatosensory-evoked potentials of the tibial nerve of a hind paw of the rat were measured to evaluate the electrophysiological function of injured spinal cord. Western blot analysis was performed to measure p38-RhoA and ERK1/2-Bcl-2 pathways related protein levels in the injured spinal cord. Rat sensory and motor functions were similar between SCI and ES groups. Compared with the SCI group, in the ES group, the latencies of the somatosensory-evoked potential of the tibial nerve of rats were significantly shortened, the amplitudes were significantly increased, RhoA protein level was significantly decreased, protein gene product 9.5 expression, ERK1/2, p38, and Bcl-2 protein levels in the spinal cord were significantly increased. These data suggest that ES can promote the recovery of electrophysiological function of the injured spinal cord through regulating p38-RhoA and ERK1/2-Bcl-2 pathway-related protein levels in the injured spinal cord.     

Spinal cord serotonin: A biochemical and immunohistochemical study following transection

The serotonin (5-HT) content of rat spinal cord was studied following complete cord transection, transverse hemisection and rhizotomy by high pressure liquid chromatography-electrochemical detection (HPLC-EC) chromatography and immunohistochemically with rabbit anti-5-HT antiserum. Spinal cord 5-HT decreased but did not disappear after complete cord transection when studied 5 or 10 days after lesioning. Indeed the indole content 5 or 10 days after section were similar. Below the transection 5-HT-like immunoreactive neuronal elements were present, appeared normal but were significantly reduced compared with control cord. Although neuronal fibers were present after transection, no immunoreactive neuronal cell bodies were observed. The neuronal elements remaining after transection were capable of synthesizing and metabolizing 5-HT as evidenced by elevated 5-HT and decreased 5-hydroxyindoleacetic acid (5-HIAA) after inhibition of monoamine oxidase. Complete cord transection resulted in a fall of 5-HT in the ventral roots suggesting that they contain efferent 5-HT elements that originate above the transection. Rhizotomy plus cord transection did not change cord indole content more than transection alone demonstrating that the indoles that remain in the cord after transection did not originate from peripheral afferent 5-HT neurons. Hemitransection resulted in partial loss of immunoreactive neuronal elements on the cut side, but 5-HT-like immunoreactive nerve fibers were observed crossing within the cord from the intact side by the spinal canal. Analysis of indole content in the hemitransected cord were consistent with crossing of 5-HT fibers within spinal segments. Our studies, taken together with reports by other laboratories, support the notion that significant 5-HT elements remain in the spinal cord after transection. These elements appear normal morphologically and biochemically.     

Changes in spinal reflex excitability in brain-dead humans

The excitability of proprio- and exteroceptive spinal reflexes was monitored electrophysiologically and clinically during the occurrence of brain death (BD) in 8 patients. After a period of total reflex unresponsiveness, the soleus H reflex attained a steady-state excitability level in 2-6 h. The recovery cycle of this response regained its normal shape at 10-20 h. The threshold of the cutaneous reflex evoked in the biceps femoris by electrical stimulation of the sural nerve had become normal in 4-13 h, although the response displayed an abnormal multi-component pattern. Digital responses to mechanical stimulation of the foot sole were evident after 6-8 h. Knee and ankle jerks were never evoked during the time of monitoring. The time-courses of the changes in excitability were not directly correlated with the fall in the blood pressure which may occur during BD. It is concluded that the human spinal cord reacts to BD with a spinal shock, characterized by sequential recovery of reflex transmission. The overall timing of this process appears to be much shorter than that previously described for the spinal shock following traumatic transection of the cord, but the latter was never studied in the earliest phases.     

Electrophysiologic and cyclic AMP changes in axon-transected frog spinal roots

Transection of a lumbar spinal nerve in the frog produces a disruption of spinal reflexes, a decrease in spinal nerve conduction velocity proximal to the lesion, and alterations in axonal cyclic AMP concentration. Conduction velocity decreases to 85% of control within 7 days of axon transection, and reaches a value 65% of control by 21 days. Monosynaptic spinal reflexes, initiated by either the descending lateral column (LC) pathway or intact lumbar dorsal roots (DRs), show a progressive increase in latency and a decrease in amplitude beginning 17 days postaxotomy. The disruption of reflex pathways continues in nonregenerating systems, but reflexes are restored to normal if regeneration occurs. The predominantly somatic terminations of the LC recover earlier than the predominantly axodendritic synapses of the DR. The signal(s) which initiates these axotomy-induced alterations in neuronal function remains to be identified. The cyclic AMP concentrations of normal and axon-transected spinal roots were measured to determine if cyclic nucleotides could play a role in this communication system. Cyclic AMP increased transiently in spinal roots 6 to 7 days after spinal nerve transection, then returned to control values and eventually began to decline 21 days postaxotomy. With the onset of regeneration, ventral root cyclic AMP concentration returned to control levels, but dorsal root concentration remained depressed. This disassociation between dorsal and ventral roots may reflect a preferential distribution of axonally transported materials into the peripheral process of the sensory axon.     

Synaptic Evoked Potentials from Regenerating Dorsal Root Axons within Fetal Spinal Cord Tissue Transplants

Previously injured dorsal roots were electrically stimulated to determine if regenerating sensory axons can form physiologically active synaptic contacts with neurons within fetal spinal cord tissue transplants. Dorsal rootlets, sectioned at their spinal cord entry zone, were apposed to intraspinal transplants of fetal spinal cord tissue grafted along each side of a nerve growth factor-treated nitrocellulose implant. Two to six months later, the rootlets were transected between the spinal cord and their respective ganglia and electrically stimulated. Evoked potentials were recorded from the dorsal surface of the transplant, but were absent from adjacent ipsilateral and contralateral spinal cord regions. A glass micropipette was advanced through the transplant and used to record intramedullary field potentials evoked by dorsal root stimulation. Maximal negative potentials occurred 400–700 μm below the dorsal surface of the transplant, shifting to positive potentials deeper into the transplant. Additionally, both spontaneous and electrically evoked single neuronal action potentials were observed along the microelectrode track. Evoked potentials were abolished following transection of the rootlets between the stimulation site and the transplant. Immunocytochemical evidence of the production of fos protein following electrical stimulation of the regenerated dorsal rootlets was demonstrated within transplant neurons and some ventrally located host neurons, providing an anatomical correlate to the electrophysiological recordings of synaptic activation. These results provide evidence of the structural and functional integration of regenerated sensory axons with both transplant and host neurons.     

Mechanisms underlying the pathogenesis of urinary bladder instability - new perspectives for the treatment of reflex incontinence

The urine storage ability of the urinary bladder is markedly impaired following inflammation of the urinary bladder and spinal cord injury because of a hyperexcitability of micturition reflexes. Using two rat models of inflammation-induced bladder overactivity and detrusor hyper-reflexia following spinal cord injury we investigated changes in the neuronal pathways to the urinary bladder which may underlie the development of this instability. Our results suggest that among the factors involved in inflammation-induced bladder instability are significant changes in the expression of the neuropeptides substance P, calcitonin gene-related peptide and galanin at the primary afferent level, as well as of the enzyme neuronal nitric oxide synthase (nNOS) at the afferent and postganglionic efferent level. In the lumbar and sacral spinal cord nNOS-immunoreactivity was depleted from dorsal horn neurones in both cystitis and spinal cord injured rats and from preganglionic parasympathetic neurones after spinal cord injury. Distension of the bladder in chronically spinalized rats elicited c-Fos expression in a significantly greater number of neurones throughout the lumbar and sacral segments than in rats with an intact neuraxis. Thus, under pathological conditions rather complicated changes in the synthesis of neuropeptides and nNOS occur at the primary afferent, spinal cord and postganglionic efferent level that together control the activity of the urinary bladder. Further mechanisms like unmasking of silent synapses and axonal sprouting in the spinal cord might further contribute to an increase in activity in micturition reflex pathways. Local cooling of the dorsal spinal cord at the level L6/S1 with temperatures between 14 and 20 degrees C proved a simple technique to control the unstable bladder and restore continence in both inflammation-induced detrusor overactivity and detrusor hyperreflexia following spinal cord injury. The effects of cooling are probably the result of a blockade of synaptic transmission within the dorsal cord which eliminates neuronal overactivity. Thus, local spinal cord cooling could offer a new method to treat bladder instability and reflex incontinence.     

Mechanisms underlying the pathogenesis of urinary bladder instability - new perspectives for the treatment of reflex incontinence

The urine storage ability of the urinary bladder is markedly impaired following inflammation of the urinary bladder and spinal cord injury because of a hyperexcitability of micturition reflexes. Using two rat models of inflammation-induced bladder overactivity and detrusor hyper-reflexia following spinal cord injury we investigated changes in the neuronal pathways to the urinary bladder which may underlie the development of this instability. Our results suggest that among the factors involved in inflammation-induced bladder instability are significant changes in the expression of the neuropeptides substance P, calcitonin gene-related peptide and galanin at the primary afferent level, as well as of the enzyme neuronal nitric oxide synthase (nNOS) at the afferent and postganglionic efferent level. In the lumbar and sacral spinal cord nNOS-immunoreactivity was depleted from dorsal horn neurones in both cystitis and spinal cord injured rats and from preganglionic parasympathetic neurones after spinal cord injury. Distension of the bladder in chronically spinalized rats elicited c-Fos expression in a significantly greater number of neurones throughout the lumbar and sacral segments than in rats with an intact neuraxis. Thus, under pathological conditions rather complicated changes in the synthesis of neuropeptides and nNOS occur at the primary afferent, spinal cord and postganglionic efferent level that together control the activity of the urinary bladder. Further mechanisms like unmasking of silent synapses and axonal sprouting in the spinal cord might further contribute to an increase in activity in micturition reflex pathways. Local cooling of the dorsal spinal cord at the level L6/S1 with temperatures between 14 and 20 °C proved a simple technique to control the unstable bladder and restore continence in both inflammation-induced detrusor overactivity and detrusor hyperreflexia following spinal cord injury. The effects of cooling are probably the result of a blockade of synaptic transmission within the dorsal cord which eliminates neuronal overactivity. Thus, local spinal cord cooling could offer a new method to treat bladder instability and reflex incontinence.     

An in vivo model to quantify motor and sensory peripheral nerve regeneration using bioresorbable nerve guide tubes

An in vivo preparation is presented to study the rate and time course of motor and sensory axonal regeneration. The cut ends of a transected sciatic nerve were inserted into each end of a 5-6 mm non-toxic and bioresorbable nerve guide tube to create a 4 mm nerve gap in adult mice. Subsequently, cell bodies in the ventral spinal cord and L3-L5 dorsal root ganglia that had regenerated axons across the gap were retrogradely labeled with horseradish peroxidase (HRP). The HRP was applied 3 mm distal to the nerve guide and was accessible only to axons that had regenerated through the nerve guide. Labeled cells were counted in 40 micron serial sections at 2, 4 and 6 weeks after initial nerve transection. The results indicate a significant increase in the number of labeled motor and sensory cell bodies over time. By 6 weeks after transection, approximately two thirds as many ventral horn motor cells and one third as many dorsal root ganglion sensory cells were labeled as in control non-transected animals. These data serve as a baseline to compare differential effects of additives to the nerve guide lumen in terms of sensory and motor neuron response.     

Intraspinal stimulation for bladder voiding in cats before and after chronic spinal cord injury

The long-term objective of this study is to develop neural prostheses for people with spinal cord injuries who are unable to voluntarily control their bladder. This feasibility study was performed in 22 adult cats. We implanted an array of microelectrodes into locations in the sacral spinal cord that are involved in the control of micturition reflexes. The effect of microelectrode stimulation was studied under light Propofol anesthesia at monthly intervals for up to 14 months. We found that electrical stimulation in the sacral parasympathetic nucleus at S(2) level or in adjacent ventrolateral white matter produced bladder contractions insufficient for inducing voiding, while stimulation at or immediately dorsal to the dorsal gray commissure at S(1) level produced strong (at least 20 mmHg) bladder contractions as well as strong (at least 40 mm Hg) external urethral sphincter relaxation, resulting in bladder voiding in 14 animals. In a subset of three animals, spinal cord transection was performed. For several months after the transection, intraspinal stimulation continued to be similarly or even more effective in inducing the bladder voiding as before the transection. We speculate that in the absence of the supraspinal connections, the plasticity in the local spinal circuitry played a role in the improved responsiveness to intraspinal stimulation.     

Responses of sympathetic postganglionic neurons to peripheral nerve stimulation in pigeon (Columba livia).

Reflex changes in heart rate and arterial blood pressure can be elicited in pigeons with high cervical transection by stimulation of brachial or lumbosacral peripheral and spinal nerves. This extends the phenomenon of spinally mediated, somatosympathetic reflexes to another vertebrate class. In a preliminary attempt to explore the spinal circuitry mediating these reflexes, the responses of single sympathetic postganglionic neurons were studied during spinal and peripheral nerve stimulation. With stimulation and recording at the same spinal segment, calculation of the central delay suggests the segmental reflex circuitry may be relatively simple, possibly trisynaptic. As the distance between stimulating and recording sites increases, postganglionic neuronal responsiveness decreases and becomes more variable. However, there is clear evidence that lumbosacral afferents can activate postganglionic neurons at brachial levels, indicating an effective propriospinal circuitry for somatosympathetic reflexes. Experiments on birds with intact spinal cords demonstrate that these spino-spinal pathways are also functional in the intact animal. While the segmental reflex is not different in the intact bird, the propriospinal pathways do behave somewhat differently, possible suggesting tonic central control.