Spinal Cord Reflexes Research Articles

Physiological studies on neuropeptides and spinal cord reflexes

Physiological studies on neuropeptides and spinal cord reflexes

Skeletal muscle tone and the misunderstood stretch reflex.

This review presents a revision of long-accepted tenets regarding the genesis of muscle tone in humans. Most discussions liken muscle tone in humans to the reflex tone described by Sherrington in decerebrate animals. That tradition presumes that muscle tone is fully determined by the monosynaptic stretch reflex, that tonic fusimotor activity is necessary for its production in normal humans, and that tonic muscle tone in antigravity leg muscles is responsible for the maintenance of posture. Data reviewed here show that nonreflex, mechanical mechanisms are involved in the maintenance of resting muscle tone; that spinal cord reflex responses are not stereotyped responses, but depend upon the ongoing activity in interneurons upon which inputs from a variety of peripheral sensory receptors and descending fiber systems converge; that long-latency transcortical responses are elicited when a muscle is stretched, and these responses effectively deal with large displacements; and that inertial components and viscoelastic muscle forces can counterbalance small amounts of body sway during quiet standing. In sum, the response to muscle stretch is not fixed and inflexible, but can be adjusted according to the demands of the moment.

The role of GABA and glycine in the physostigmine-induced alterations of spinal cord reflexes

The purpose of this study was to determine which inhibitory pathway(s) mediate the alterations in the monosynaptic (MSR) and polysynaptic (PSR) reflexes after two different doses of physostigmine. It was found previously that 0.8 mg kg physostigmine facilitated the MSR and 2.0 mg kg initially depressed and then facilitated the MSR. Both doses facilitated the PSR. In this study, the animals were pretreated with either strychnine (0.1 mg kg ) or bicuculline (0.5 mg kg ), prior to the administration of either dose of physostigmine. It was found that both strychnine and bicuculline blocked the facilitation produced by the small dose of physostigmine, while bicuculline alone blocked the depression of the MSR produced by the large dose of physostigmine. Strychnine partially blocked the effects of both doses of physostigmine on the PSR, while bicuculline only partially blocked the effects of the small dose of physostigmine. These data suggest that the depression of the MSR was the result of a GABA-mediated pathway, while the facilitation of MSR involved both glycine and GABA.

Effects of Naloxone and Levallorphan on the Spinal Cord Reflex Potentials under the Spinal Ischemic Condition in Cats

The spinal reflex potentials elicited by electrical stimulation of the tibial nerve were recorded from the lumbo-sacral ventral root in spinal cats. When the thoracic aorta and the bilateral internal mammary arteries were occluded for 10 min, the potentials were completely depressed. Reappearance of these potentials could be observed at about 10 min after removal of the occlusion and they gradually recovered. Intravenous injection of naloxone (1 or 10mg/kg) or levallorphan (0.1 mg/kg) together with removal of occlusion significantly promoted the recovery of the polysynaptic reflex potential. Morphine (5 mg/kg) showed no particular effect on the recovery of potentials. Furthermore, pretreatment with morphine (5 mg/kg) did not influence the effects of these opioid antagonists. These results suggest that naloxone and levallorphan may preserve or potentiate the intemeuronal activities of the lumbo-sacral spinal cord under the ischemic condition and that the effects may not be mediated through morphine-like opioid receptors.

Aspects of Spinal Cord Structure and Reflex Function

Current textbooks still feature overly simplistic approaches to spinal cord function. Medical training still emphasizes the notion of stereotyped spinal reflex responses fixed by rigid neuronal connections. These assumptions must be replaced by recognizing (1) that descending and sensory information converges on the same sets of interneurons, (2) that the effects of different classes of afferents from muscle, joints, and skin act together in different combinations as a result of convergence, (3) that the flexibility of reflex responses is determined in large measure by the excitability of interneurons, (4) that conventional and monoamine transmitters act and interact to adjust neuronal excitability and transmission in reflex pathways, and finally (5) that rhythmic movements are largely determined by intraspinal circuitry.

Effects of acute administration of soman on spinal cord reflexes in the cat

The acute effects of the organophosphorus acetylcholinesterase inhibitor, soman, was studied on spinal cord reflexes in the spinal cord transected cat. It was found that doses of 10 μg/kg significantly altered the monosynaptic and dorsal root reflexes by causing an initial depression lasting about 20 min followed by a later facilitation lasting over 3 h. A higher dose of soman (20 μg/kg) caused the initial depression but did not produce the later facilitation. Cholinergic antagonists were used to determine whether these changes were related to inhibition of acetylcholinesterase or whether they were non-specific. It was found that mecamylamine blocked the depression and the facilitation while atropine depressed the spinal cord potentials. These data show that acute administration of 10 μg/kg soman produces specific effects on spinal cord reflexes which could be characterized as resulting from inhibition of acetylcholinesterase similar to the carbamate inhibitor, physostigmine.

A simplified organ donor model produced by permanent complete central nervous system ischemia in dogs

The physiologic and pathophysiologic changes of the potential organ donor in the brain-dead state are poorly understood. We have developed a canine model of complete brain death by infusing saline into the subdural space and elevating intracranial pressure above systolic arterial pressure. A snare on the inferior vena cave decreased venous return and limited the Cushing response to 1 to 2 minutes. The electroencephalogram became isoelectric as soon as intracranial pressure was elevated and maintained above systolic arterial pressure. The brain-dead state was confirmed by several means. No return of electroencephalogram activity was seen throughout the study. Neurologic examination failed to document any cranial nerve or spinal cord reflexes after the induction of brain death. Pharmacologic challenges failed to document any baroreceptor function or autonomic cardiovascular control in this state. Blood flow to the central nervous system using the microsphere technique was determined at 1 hour post-brain death. The mean calculated flows were not statistically different than zero. The model provides a simple, controlled, consistent, and relatively noninvasive model of complete brain death. It should facilitate the investigation of the mechanisms leading to somatic death in the brain-dead state and ultimately lead to improved clinical supports.

Erratum: Changes in spinal cord reflexes after cross-anastomosis of cutaneous and muscle nerves in the adult rat

Erratum: Changes in spinal cord reflexes after cross-anastomosis of cutaneous and muscle nerves in the adult rat

Changes in spinal cord reflexes after cross-anastomosis of cutaneous and muscle nerves in the adult rat.

Evidence exists that the specification of afferent nerves and their central connections in the embryo may depend in part on influences from the peripheral target innervated. We have now investigated whether such peripheral determination persists in the adult rat using the unmyelinated afferent system of C fibres, which differ chemically in the adult depending on their target. We have previously shown that if the cutaneous sural nerve and the muscle gastrocnemius nerve are cross-anastomosed so that they grow to each other's target, the A fibres establish functional endings and the C fibres change their chemistry to that which is appropriate for the new target. Here we report that in normal adult rats, a short train of stimuli to the cutaneous sural nerve produced a brief facilitation of the flexion reflex, lasting on average only 5 min, whereas similar stimulation of the gastrocnemius-muscle nerve enhanced this reflex for an average of 54 min. In cross-anastomosed animals, stimulation of the gastrocnemius nerve (innervating skin) induced a brief potentiation of the flexion reflex, lasting on average only 3 min. By contrast, stimulation of sural nerve (innervating muscle) produced a potentiation of this reflex lasting 57 min. Thus the ability of adult afferent nerves to potentiate the flexion reflex depends on the target with which they make contact. We propose that tissue-specific factors influence some of the central actions of primary afferent neurons in the adult.

Electrophysiological evidence for nicotinic and muscarinic modulation of spinal cord reflexes

Intravenous administration of physostigmine has been found to produce dose- and timedependent alterations of the lumbar monosynaptic and polysynaptic reflexes in spinal cats. A small dose of physostigmine (0.8 mg/kg) enhanced the monosynaptic reflex for 3 hr, while a larger dose (2.0 mg/kg) produced a pattern of initial depression which peaked at 5 min, followed by an increase which was maintained for 3 hr after injection. Both doses of physostigmine were found to produce a similar pattern of enhancement of the polysynaptic reflex. Atropine and mecamylamine antagonized the increase of the monosynaptic reflex produced by both doses of physostigmine. The initial depression of the monosynaptic reflex produced by the large dose of physostigmine was blocked by mecamylamine, but unaffected by atropine. The enhancement of the polysynaptic reflex, produced by both doses of physostigmine, was antagonized by atropine but not by mecamylamine. In addition, nicotine and oxotremorine were found to mimic the initial effects of physostigmine in the presence of the appropriate antagonist. These data show that both muscarinic and nicotinic receptors are involved differentially in the modulation of spinal reflexes and that physostigmine had an additional late effect which consistently occurred at 20 min after administration.

Descending catecholaminergic modulation of spinal cord reflexes in cat and rat.

Annals of the New York Academy of SciencesVolume 563, Issue 1 p. 45-58 Descending Catecholaminergic Modulation of Spinal Cord Reflexes in Cat and Rata CHARLES D. BARNES, CHARLES D. BARNES Department of VCAPP Washington State University Pullman, Washington 99164Search for more papers by this authorSIMON J. FUNG, SIMON J. FUNG Department of VCAPP Washington State University Pullman, Washington 99164Search for more papers by this authorOTTAVIO POMPEIANO, OTTAVIO POMPEIANO Dipartimento di Fisiologia e Biochimica Universita di Pisa 56100 Pisa, ItalySearch for more papers by this author CHARLES D. BARNES, CHARLES D. BARNES Department of VCAPP Washington State University Pullman, Washington 99164Search for more papers by this authorSIMON J. FUNG, SIMON J. FUNG Department of VCAPP Washington State University Pullman, Washington 99164Search for more papers by this authorOTTAVIO POMPEIANO, OTTAVIO POMPEIANO Dipartimento di Fisiologia e Biochimica Universita di Pisa 56100 Pisa, ItalySearch for more papers by this author First published: June 1989 https://doi.org/10.1111/j.1749-6632.1989.tb42189.xCitations: 7 a Most of the research from the authors' laboratories reported in this review was supported by NIH Grants NS 17040 and NS24388 (CDB) and 07685 (OP). AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume563, Issue1Modulation of Defined Vertebrate Neural CircuitsJune 1989Pages 45-58 RelatedInformation

Changes in spinal cord reflexes following subchronic exposure to soman and sarin

The organophosphorus agents soman and sarin were administered subchronically and the spinal monosynaptic (MSR) and dorsal root (DRR) reflexes were assessed in spinal cord-transected cats. Neither soman nor sarin produced behavioral signs of delayed neurotoxicity. However, both soman and sarin significantly reduced the area under the MSR and DRR with only minimal changes in the excitability of the potentials as determined using quipazine, a serotonin agonist. The changes observed in these reflexes resulting from soman or sarin exposure are discussed in relation to alterations in the central terminals of primary afferent neurons.

Functional corticotropin-releasing factor receptors in neonatal rat spinal cord

The present study localized corticotropin-releasing factor (CRF) receptors and studied the action of CRF in the neonatal rat spinal cord preparation. Lumbar CRF receptors were present in highest concentrations in laminae I and II with progressively lower concentrations in lamina IX and intermediate and central zones respectively. CRF directly and indirectly depolarized lumbar motoneurons in a concentration-related manner and the putative receptor antagonist, alpha helical oCRF(9-41), partially blocked the depolarizing response to CRF. The electrophysiological responses to CRF and the distribution of receptors within the spinal cord suggest that CRF may play a physiological role in regulating spinal cord reflex function.

Synaptic physiology of spinal motoneurones of normal and spastic mice: an in vitro study.

Spinal cord reflexes have been examined in a preparation of the mouse spinal cord maintained in vitro. Responses of the motoneurone population of normal and spastic mutant mice to stimulation of a segmental dorsal root were compared. In the normal spinal cord, a monosynaptic response with very little polysynaptic excitation was typical. In the mutant, the monosynaptic response was typically followed by a depolarizing wave on which asynchronous compound action potentials were superimposed. In some spastic cords, an oscillating depolarizing wave was seen, lasting up to 500 ms. The stimulus range from threshold to maximal response was the same for the normal and mutant. The dorsal root reflex (d.r.r.) and dorsal root potential (d.r.p.) were prominent in both normal and mutant, and no consistent difference could be identified. Intracellular recordings were made from motoneurones using electrodes filled with potassium acetate. Mean resting potentials and input resistances were not significantly different in mutant and normal mice. The voltage-dependent conductances, seen as the after-depolarization and after-hyperpolarizations following antidromic action potentials and the responses of motoneurones to depolarizing current injection were similar in both populations. The synaptic responses of motoneurones following stimulation of the segmental dorsal root were clearly abnormal in the mutant. In the normal mice, a monosynaptic excitatory post-synaptic potential (e.p.s.p.), seen at low stimulus intensities, was followed at higher stimulus intensities by polysynaptic activity lasting up to 100 ms, which rarely reached threshold for action potential discharge. In the mutant mice, the monosynaptic response was typically followed by depolarizing synaptic responses which often evoked action potentials before the monosynaptic response reached threshold. At higher stimulus intensities, the monosynaptic response was followed by at least one and often multiple action potentials generated on prolonged depolarizing synaptic activity. When cells were impaled with potassium-acetate-filled electrodes, very little spontaneous synaptic activity was seen in either normal or mutant mice. Spontaneous depolarizing post-synaptic potentials (p.s.p.s) were prominent in normal motoneurones when potassium chloride was used to fill electrodes and were increased in amplitude by ionophoresis of chloride into the cells. Under these conditions stimulation of a ventral root evoked a depolarizing p.s.p. and the Renshaw i.p.s.p. reversed. The spontaneous p.s.p.s were blocked by ionophoresis or bath application of the glycine antagonist strychnine.(ABSTRACT TRUNCATED AT 400 WORDS)

Paradoxical changes in spinal cord reflexes following the acute administration of acrylamide

Acrylamide (ACR) produces a central-peripheral distal axonopathy when administered chronically. This is characterized functionally by decreases in the monosynaptic reflex (MSR) and dorsal root potential (DRP) and alterations in the characteristics of the dorsal root reflex (DRR). Acute administration of ACR inhibits the oxidative enzyme complex NADH-tetrazolium reductase and slows retrograde axoplasmic transport. This study was carried out to determine if the spinal cord reflexes are also affected following acute administration of ACR. Dose-response studies revealed a dose-dependent increase in both the MSR and DRR. A single injection of 50 mg/kg ACR caused an increase in both the MSR and DRR within 15 min and continued for over 3 h. These data are paradoxical since chronic administration of ACR results in decreased function. Two possible mechanisms are proposed. First, calcium ion regulation may be involved in both the acute and chronic effects of ACR on spinal cord reflexes. Second, a depolarization of the neurons is occurring just prior to cell injury or death.

Catheter-induced hyperreflexia in spinal cord injury patients: diagnosis by sonographic voiding cystourethrography.

In part 1 of this study, 77 consecutive patients with spinal cord injuries and reflex bladders were examined by combined urodynamic studies and sonographic voiding cystourethrography. Of the 15 (19%) who had hyperreflexic bladders (reflex bladders that contracted when containing 125 ml or less), eight (53%) had catheter-induced hyperreflexia (proved by sonographic voiding cystourethrography without catheterization). The significant overdiagnosis influenced patient care because catheter-induced hyperreflexia did not require treatment, whereas primary hyperreflexia caused by lesions above T-5 always required anticholinergic therapy to prevent potentially life-threatening autonomic dysreflexia. In part 2 of this study, 116 additional spinal cord injury patients with reflex bladders were studied, although in these patients the catheter was introduced under sonographic control. Seven (6%) of these patients had hyperreflexia, but in none was the hyperreflexia catheter induced, showing that use of sonography while introducing the catheter can prevent catheter-induced hyperreflexia.

Periodic leg movements of sleep (nocturnal myoclonus): an electrophysiological study.

Six patients with periodic leg movements of sleep (PLMS) were studied electrophysiologically. All patients had normal results on routine nerve conduction studies and electromyography. In 5 patients the blink reflex consisted of three components, and in 1 patient it consisted of four components, with two components being normal. The second component of their blink reflex did not habituate. Other abnormalities included long-latency responses in the extremities in 2 patients, release of H-reflexes from flexor hallucis brevis muscle in 2 patients, and an Hmax/Mmax ratio of 98% in 2 patients. One patient's median nerve somatosensory-evoked response had a markedly enlarged P22 wave. These electrophysiological abnormalities suggest a disorder of the central nervous system producing increased excitability of segmental reflexes. To produce increased excitability of both brainstem and spinal cord reflexes, the disorder must be operative at the pontine level or rostral to it. Since long-latency components of blink reflexes occurred in all our patients, this may be a helpful diagnostic test when PLMS is suspected.

Thigh muscle activity during maximum-height jumps by cats.

Cats were trained to jump from a force plate and touch a cotton ball suspended as high as 1.6 m. Force-plate reaction forces and double-joint hamstring muscle activity observed early in propulsion varied from one maximal jump to another. This variability is consistent with theory (31, 32, 42); that is, different coordination strategies can be implemented prior to the heels losing contact with the force plate (heel-off). Single-joint hip extensor and double-joint posterior thigh (hip extensor-knee flexor) muscles were coactivated prior to heel-off. This coactivation is probably partially responsible for the observed backward rotation of the trunk. Forepaws, observed to contact the force plate prior to heel-off, probably assist the hindlimbs in generating trunk rotation. Both single-joint knee extensor and hip extensor muscles exhibited greatest activation between heel-off and body lift-off. Single-joint flexor muscles were inactive throughout propulsion. Double-joint posterior thigh muscles were deactivated at heel-off and remained inactivated until lift-off. These observations agree with the theoretical notion that muscles should be either fully activated, inactivated, or switched from one extreme to the other (i.e., bang-bang control) between heel-off and body lift-off (31, 32, 42, 44). All seven muscles studied shortened while activated. Using computations based on muscle geometry, fiber architecture, and joint angle trajectories, I propose that sarcomeres shorten along the flat and ascending regions of the force-length curve. De- and inactivation of double-joint posterior thigh muscles between heel-off and lift-off coincided with muscle stretch. The reason for inactivation of these muscles is that the negative work that would have been generated had these muscles stayed activated would have hindered propulsion. Contractions preceded by active stretch were not observed. Enhancement of positive work by previous storage of energy in elastic musculotendinous structures is thus not used by cat thigh musculature in jumps starting from the squat. Adductor femoris, semimembranosus anterior, and biceps femoris anterior muscles were activated synergistically as one group yet differently from the synergistic activation of gracilis, semitendinosus, and biceps femoris posterior muscles. The separation of these muscles into two groups based on their activation patterns during jumping is compatible with the classification of these muscles into hip extensor and knee flexor muscle groups, respectively, based on their reflex patterns (37), spinal cord reflex connectivity (18, 30), and firing patterns during locomotion (20).(ABSTRACT TRUNCATED AT 400 WORDS)

Temporal pulmonary function changes in cervical cord injury.

Temporal changes in pulmonary function (PF) in subjects with complete cervical cord transection occur in two stages. The first, extending from the acute to post-acute periods, is characterized by relatively rapid increases in the following: vital, inspiratory, and total lung capacities (VC, IC, and TLC, respectively), and inspiratory and expiratory airflows coupled with decreases in functional residual capacity (FRC). Second stage changes--from the post-acute period on--are more gradual, with both VC increase and FRC decrease continuing while TLC and ventilatory indices remain unchanged. The initial stage appears to be caused in part by functional respiratory muscle return coincident with resolution of inflammation and edema above the injury level. Altered respiratory mechanics also contribute to these early changes and the continuing later changes. Mechanical changes in the lung are probably both decreased compliance (which decreases FRC) and increased airway resistance (which diminishes airflow). Chest wall changes, resulting from returning spinal cord reflexes, affect PF via: (1) increased rib cage stability, leading to a more effective transduction of diaphragmatic displacement into lung volume, and (2) abdominal and expiratory intercostal spasticity, which could limit maximum inspiration. The net effect of these changes, however, may eventually lead to chronic hypoventilation.

Descriptive studies of H-reflex recovery curves in psychiatric patients.

The rate of recovery of the H-reflex, an electrical evoked monosynaptic spinal cord reflex, was abnormally high (fast) in over 20% of unmedicated psychotic patients of all major diagnostic classes. A few patients had significantly lower H-reflex recovery curves. Chronic neuroleptic treatment produced relatively lower recovery curves, whereas fluoxetine, a specific serotonin uptake blocker, produced relatively higher curves.