Spinal Section Research Articles

Maintenance of specificity by sprouting and regenerating peripheral nerves. II. Variability after lesions

In previous studies we showed that collateral sprouting in cat tibialis anterior (TA)k muscle was elicite by selective peripheral spinal nerve section sparing L 7. After chronic (3 week) section of L 5, L 6, S 1 and S 2 spinal nerves in the present study, two different reflex patterns were observed. In some cats, with presumed prefixation of the lumbosacral plexus, the TA tendon reflex was weakened initially and became stronger beginning 2–3 days postoperative. In other cats, with presumed postfixation of the plexus, the TA tendon reflex was abolished for 7–9 days and then returned. The TA muscles were injected with HRP and labeled motor neurons plotted. In the ‘prefixed’ first group, the number, location and size of motor neurons projecting to TA through the spared L 7 nerve were symmetrical when acute and chronic sides were compared. In the ‘postfixed’ group (reflex abolished then returned) the acute and chronic sides were asymmetrical: the chronic side displayed a significant increase in number of labeled cells and an increase in the rostocaudal extent of the cell column within the L 7 segment. These results are consistent with two types of collateral sprouting: homonymous, in which the sprouts arise from nerves within the muscle, and heteronymous, in which the sprouts arise from nerves in adjacent muscles. In animals with very chronic (up to 2 years) spinal nerve section (L 5, L 6, S 1 and S 2) regeneration of the cut nerves was superimposed on the spared L 7 innervation. Topography was completely disrupted except in the L 7 segment. Thus, there appears to be a difference in specificity of motor neurons for target sites depending upon degree and location of denervation. Homonymous sprouting displays strict specificity, regeneration does not and heteronymous sprouting represents an intermediate form in which cells are recruited from adjacent motor neuron pools in the segment of the spared innervation.

Role of vagal and spinal sensory pathways in diaphragmatic response to resistive loading

The effects of severe inspiratory (I) or expiratory (E) resistive loads on diaphragmatic activity were studied in two groups of cats anaesthetized with sodium pentobarbital or ethylcarbamate-chloralose. In intact cats, I or E loading never changed the amplitude of integrated diaphragmatic electric myogram (EMG) measured at 1.0 s (Edi 1.0); only I loading, prolonged the duration of diaphragmatic activity (Tdi). After selective procaine block of non-volume related vagal sensory inputs, I or E loading markedly increased Edi 1.0 and changes in Tdi due to I loading persisted. After bivagotomy, which also suppressed volume related vagal feed back, Edi 1.0 increased during I or E loading but change in Tdi disappeared. Initial spinal section at C 8 level only reduced changes in Tdi with inspiratory loading. Bivagotomy plus spinal section abolished all load induced changes in diaphragmatic activity. These results suggest that all vagal information from the lungs participate in the mechanism of load compensation but that spinal sensory pathways play a minor role in this response in anaesthetized cats.

Role of vagal and spinal sensory pathways on eupneic diaphragmatic activity.

The interactions between vagal and spinal afferents in the control of eupneic diaphragmatic activity were studied in two groups of cats anesthetized either with pentobarbital sodium (SPB) or with ethyl carbamate-alpha-chloralose (ECC), which enhanced spinal reflexes. Under both conditions of anesthesia two experimental protocols were performed: 1) bilateral cervical vagotomy followed by spinal section at C8 level or 2) spinal section followed by vagotomy. Changes in integrated diaphragmatic activity (Edi) were studied during eupneic ventilation and tracheal occlusion at end expiration. Vagotomy always significantly increased the amplitude of Edi during eupnea (SPB + 30%; ECC + 15%) and prolonged its duration (Tdi) (SPB + 110%; ECC + 75%) but did not modify the overall shape of the Edi vs. time relationship. Spinal section induced reverse changes in the amplitude of Edi, whether vagal afferents were present or suppressed and modified the shape of the Edi wave, but did not significantly modify Tdi. These results indicate that both vagal and spinal afferents may participate in the control of eupneic inspiration but exert different and interdependent influences on the recruitment and firing time of phrenic motoneurons. In addition, Tdi measured during tracheal occlusion (Todi) was markedly prolonged under ECC anesthesia. In this situation spinal section reduced Todi, which became close to the values obtained in intact or spinal cats under SPB anesthesia. Thus the response to tracheal occlusion at end expiration cannot be interpreted as resulting from the sole suppression of volume related vagal information.

Ascending pathways in the spinal cord involved in triggering of diffuse noxious inhibitory controls in the rat.

Recordings were made from convergent neurons in trigeminal nucleus caudalis of the rat. These neurons were activated by both innocuous and noxious mechanical stimuli applied to their excitatory receptive fields located on the ipsilateral part of the muzzle. Transcutaneous application of suprathreshold 2-ms square-wave electrical stimuli to the center of the excitatory field resulted in responses to C-fiber activation being observed (mean latencies 63.6 +/- 5.5 ms). This type of response was inhibited by applying noxious conditioning stimuli to heterotopic body areas, namely immersing either the left or right hindpaw in a 52 degrees C water bath. A virtually total block of the response was observed during the application of the noxious conditioning stimulus, and this was followed by long-lasting poststimulus effects. Such inhibitory processes have been termed diffuse noxious inhibitory controls (DNIC) (39, 40). The effects on these inhibitions of various transverse lesions of the cervical spinal cord were investigated in acute experiments; tests were performed before and at least 30 min after the spinal section. While the unconditioned C-fiber responses were unaltered, the inhibitory processes could be impaired by the cervical lesions, although these effects depended on the part of the cervical cord destroyed and the side of application of the conditioning stimulus. Lesioning dorsal, dorsolateral, and ventromedial parts of the cervical cord was found not to affect inhibitory processes triggered from either hindpaw. The overlapping of the regions of these ineffective lesions revealed that two remaining regions were not destroyed, that is, the left and right ventrolateral quadrants. In experiments where the left anterolateral quadrant was affected by the surgical procedure the inhibition triggered from the right hindpaw was strongly reduced, whereas that elicited by left hindpaw stimulation was not diminished. The loss of inhibitory effects was characterized by a complete disappearance of poststimulus effects, whereas inhibition observed during the application of the noxious thermal conditioning stimulus was only partially, albeit very significantly, blocked. To ascertain further the mainly crossed nature of the pathways responsible for the heterotopic inhibitory processes, the effects of lumbar commissurotomy were investigated. Again the unconditioned C-fiber responses were unaltered by this procedure, whereas the inhibitory processes, whether triggered from the left or right hindpaw, were strongly depressed in all the experiments.(ABSTRACT TRUNCATED AT 400 WORDS)

Cardiorespiratory changes following chemical applications to gut serosa

Application of 0.2–0.3 ml of 1 M ammonium chloride, 100 mM citric acid, 100 mM hydrochloric acid, 1% potassium chloride, 1% ammonium oxalate, 1% oxalic acid, 0.5% sodium hydroxide, 200 μg% bradykinin or 20 mg% capsaicin to gastrointestinal serosa produced a fall in blood pressure and inhibition of respiration in hypertensive as well as normotensive rats. In 6 (8%) of the animals studied, a fall in heart rate was also seen which was blocked by atropine. The blood pressure changes were independent of changes in heart rate. After acute abdominal vagotomy, while the respiratory inhibition following chemical application on gut serosa was enhanced, the cardiovascular responses were the same as before. In animals subjected to sympathetic denervation by spinal section at T5, celiac ganglionectomy or splanchnicotomy, a similar application produced an augmented respiratory response while the cardiovascular parameters were unaffected. These results show that the above inhibitions were mediated through the sympathetic afferents and a minor stimulation of respiration, via vagal afferents. The efferent pathway for the cardiac changes seems to be via vagus and the vascular changes via the sympathetics. In chronic vagotomized animals, the same stimulation produced a response similar to that seen in animals with intact vagus. An adaptive response may be operating in chronic animals reverting the status back to normal.

Analysis of the heart rate effects of 5-hydroxytryptamine in the cat; mediation of tachycardia by 5-HT1-like receptors.

The effects of 5-hydroxytryptamine (5-HT) on heart rate in anaesthetized cats were analysed both in intact animals and after spinal section plus vagotomy. The intact cat responded to 5-HT (3, 10 and 30 micrograms X kg-1, i.v.) with a brief, but intense, bradycardia and a longer-lasting hypotension. Administration of MDL 72222, a selective antagonist of M-type 5-HT receptors, blocked bradycardia elicited by 5-HT without affecting that caused by stimulation of the vagus nerve. In spinal cats the same doses of 5-HT increased heart rate and blood pressure. These effects remained essentially unchanged after bilateral adrenalectomy, guanethidine, propranolol and burimamide, suggesting that 5-HT acted directly on the myocardium and blood vessels. The tachycardic responses to 5-HT in spinal cats were little affected by 0.5 mg X kg-1 doses of MDL 72222 or of the 5-HT2 receptor antagonists, ketanserin, ritanserin or cyproheptadine. In contrast, the non-selective 5-HT receptor antagonist, methysergide, which binds to both 5-HT1 and 5-HT2 recognition sites in rat brain membranes, potently antagonized the 5-HT-induced tachycardia in doses of 0.05 to 0.5 mg X kg-1. However pizotifen and mianserin, two other 5-HT2 antagonists which show poor affinity for 5-HT1 recognition sites, were also effective against the tachycardic response to 5-HT in doses of 0.5-4.5 mg X kg-1. The pressor responses to 5-HT in the spinal cat were markedly inhibited by all six 5-HT2 antagonists at a dose of 0.5 mg X kg-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Potentiels de moelle lombaire evoques par stimulation des nerfs du membre inferieur chez l'homme

Lumbar cord potentials evoked by electrical stimulation of the posterior tibial and sural nerves at the ankle were recorded with monopolar epidural electrodes, at T11-T12 level in 20 subjects and were compared with surface recorded potentials. Two quadriplegic patients with spinal section were included in this group. Curare was given in two cases. Xylocaine block of peripheral nerve was carried out in 4 cases. Double shock study was done in 5 cases. The lumbar cord evoked potentials show two successive components: a 'primary' negative-positive spike response with a latency of 19-35 msec, and the 'secondary' waves with latencies up to 200 msec. The 'primary' response is mainly produced by the afferent volley in the fibres of the dorsal roots and of their intramedullary prolongations. There is no evidence which suggests that it is correlated with presynaptic inhibition. The secondary components may be divided into the early and the late waves. The early waves (40-90 msec) are related to the polysynaptic activities from the afferent fibres of small diameters. The late waves are under the influence of supraspinal mechanism and may be related to long-loop reflexes. The clinical implications of these evoked potentials are discussed.

The hepatic vagus nerve and the neural regulation of insulin secretion.

Despite considerable evidence that vagal neural efferent pathways between brainstem and pancreatic islets may alter the secretion of insulin, afferent pathways which might affect this system have received little attention. In the present work we have examined the effects on plasma insulin concentration of several treatments designed to alter the neural activity of the hepatic vagus nerve, a major afferent pathway between the liver and the medulla. The hepatic vagus nerve was acutely sectioned or stimulated electrically in separate experiments in rats. In a third experiment, glucose or 3-O-methylglucose was given ip to stimulate or inhibit, respectively, the hypothetical hepatic glucoreceptors. The effects of these treatments were assessed by measuring arterial or portal plasma insulin concentrations. Anesthesia and its possible secondary inhibitory effects on insulin secretion were avoided by a spinal sectioning of the rats in the cervical region, before experimentation. Acute section of the hepatic vagus nerve between the liver and the main anterior vagal trunk caused an increase in both arterial and portal plasma insulin concentrations. Stimulation of the central end of the nerve suppressed the concentration of the hormone in both the arterial and portal plasma relative to sham-stimulated controls. Section of the celiac vagal branches to the pancreas abolished these changes. Intraperitoneal glucose enhanced arterial insulin more in sham-vagotomized than in hepatic-vagotomized rats. After 3-O-methylglucose was given ip, the response was the opposite: insulin rose more in the arterial plasma of the hepatic-vagotomized animals than in those sham vagotomized. These results suggest that the hepatic vagus nerve plays a role in the regulation of insulin secretion. They are consistent with the hypothesis that afferent fibers in this nerve exert a tonic inhibition on the brainstem centers of an efferent vagal pancreatic neuroendocrine system.

Differential effects of transection of the spinal cord and splanchnic nerve on adrenal tyrosine hydroxylase and catecholamines

The role of spinal pathways in the regulation of adrenal medullary tyrosine hydroxylase and catecholamines was studied in adult rats subjected to spinal cord transection at the third thoracic level. In these animals the sympathoadrenal preganglionic neurons were isolated from their supraspinal afferents. This treatment led after three days to a progressive reduction of tyrosine hydroxylase activity and dopamine content (as compared to unoperated controls) until at least the 10th day. The results of the administration of dexamethasone or adrenocorticotropic hormone to spinalized rats suggest that in these animals glucocorticoid hypersecretion is not involved in the decline of adrenal tyrosine hydroxylase and that in fact adrenocorticotropic hormone supplementation can prevent it. A neurogenic origin for the depression of adrenomedullary function is favoured because unilateral splanchnicotomy (which by itself does not affect adrenal tyrosine hydroxylase), prior to cord section, prevented the diminution of tyrosine hydroxylase activity in the denervated gland. The decline of adrenal tyrosine hydroxylase and dopamine after spinal section may result from a decrease of modulatory impulses to the adrenal from decentralized sympathoadrenal preganglionic neurons in the isolated cord, following the loss of a descending facilitation of these neurons and/or the release of a segmental interneuronal inhibition of these neurons from a descending inhibitory influence. Such descending pathways may decussate partially below the low cervical level because rats with hemisection of the cord at C 6-C 7 exhibited no decline of adrenal tyrosine hydroxylase or of dopamine measured on either side seven days postoperatively.

Long-term retention of a peripherally induced flexor reflex alteration in rats

The long-term nature of peripherally induced spinal fixation was examined in the present study. Sixty-three anesthetized rats received 45–90 min of hindlimb stimulation. After a 24–72 h waiting period, the animals were given a midthoracic spinal section and hindlimb asymmetry was assessed. Our results indicate that a compensatory mechanism was activated after stimulation to correct the postural imbalance. Long-lasting effects of stimulation were manifested, however, when the compensatory influence was eliminated by spinal section.

Blood pressure response to Ro15-1788, a benzodiazepine antagonist

The effects of Ro15-1788, a benzodiazepine antagonist, on heart rate and blood pressure were studied in chloralose anesthetized cats. In previously untreated controls, Ro15-1788 lowered both systolic and diastolic arterial pressure about 15 mm Hg, and slightly decreased heart rate. In cats that had been given a single acute dose of diazepam or flurazepam, Ro15-1788 increased blood pressure about 40 mm Hg. A similar increase was measured in cats that were tolerant and physically dependent after 5 weeks of chronic flurazepam treatment. High spinal (C-1) section abolished all Ro15-1788 effects. It is suggested that the observed drug actions occur within the CNS rather than in the periphery, and that it might be useful to study further the cardiovascular actions of benzodiazepine agonists and antagonists.

Spinal and cortical evoked potentials following stimulation of the posterior tibial nerve in the diagnosis and localization of spinal cord diseases

Evoked potentials from unilateral stimulation of the posterior tibial nerve at the ankle were recorded over the spinous processes L5, L1, C2 and Cz′ in 30 normal subjects (Table Ia, b and c), 11 patients with multiple sclerosis (Table II) and 8 patients with a proven space-occupying spinal cord lesion (Table III). Delayed sensory conduction of both absolute latencies and side to side differences of P40 was seen in 91% of MS patients. Additional recording of spinal evoked potentials over L5, L1 and C2 did not significantly increase the percentage of abnormal responses. The spinal cord evoked responses therefore have their diagnostic importance in localizing the demyelinating process to the spinal or supraspinal section of the sensory pathway and in excluding peripherally delayed impulse conduction. The absolute latencies were within normal limits or only slightly delayed in the spinal tumor group. The interpeak latencies between the lumbar and the cervical or cortical responses showed less variability as compared to the absolute ones and revealed slight delays in some cases. Diagnostically more important seems the amplitude quotient between the cortical and the lumbar evoked potentials (P40/S response) which was below the normal range in two thirds of the tumor group patients.

Effect on arterial pressure of rhythmically contracting the hindlimb muscles of cats.

Although static contraction of the hindlimb muscles of anesthetized cats is known to reflexly increase arterial pressure and heart rate, the cardiovascular effects of rhythmic contractions of these muscles is unclear. To help clarify this issue, we determined, in chloralose-anesthetized cats, the effects on arterial pressure and heart rate of rhythmically contracting the hindlimb muscles at a frequency of 5 Hz. In addition, we determined the effect of rhythmic contractions on the impulse activity of group III and IV muscle afferents whose activation is known to increase cardiovascular function. We found that rhythmic contractions increased arterial pressure (from 108 +/- 8 to 134 +/- 9 mmHg; P less than 0.05) and heart rate (from 192 +/- 13 to 208 +/- 10 beats/min; P less than 0.05) in 10 cats and decreased arterial pressure (from 107 +/- 8 to 93 +/- 9 mmHg; P less than 0.05) but did not change heart rate in 9 other cats. The increases were reflex, because they were prevented by cutting the spinal roots innervating the contracting hindlimb. The decreases, however, were not reflex, because they persisted after spinal root section. The differences in the arterial pressure responses to rhythmic contractions may have been partly due to individual differences in the level of anesthesia, because in three cats the pressor responses to this maneuver were converted to depressor responses after giving the cats additional chloralose. Rhythmic contractions of the triceps surae muscles stimulated 8 of 10 group III afferents and 9 of 16 group IV afferents. We conclude that rhythmic contraction is capable of reflexly increasing cardiovascular function in cats provided that the effect is not depressed by anesthesia.

Centrally-induced vasopressor responses to carbachol are augmented in DOCA-salt hypertensive rats.

Increased sympathetic nervous system activity and vasopressin release has been demonstrated in established DOCA-salt hypertension in the rat. To determine the importance of these mechanisms in centrally-mediated pressor responses in this model of hypertension, both awake rats and rats anaesthetised with urethane were given intracerebroventricular injections of carbachol. The systolic blood pressure after implanting a silicon rubber mould containing DOCA, and with subsequent substitution of 1% saline in tap water, increased from 112 +/- 3 mmHg to a stable 188 +/- 7 mmHg by the end of 4 weeks, measured using a tail-cuff method. The blood pressure consistently became elevated when carbachol was injected into the cerebral ventricles of awake rats. Of the three groups of normotensive rats (NTR), sham-operated rats (SHAM) and DOCA-salt hypertensive rats (DOCA), the magnitude of the pressor phase was largest in the DOCA rats. The heart rate in all three groups of rats decreased similarly. When the rats were later anaesthetised with urethane to allow recording of abdominal sympathetic nerve activity, the carbachol injections caused biphasic blood pressure responses and sympathetic nerve discharge consisting of initial vasodepression and sympathetic nerve inhibition of short duration. This was followed by a sustained pressor phase accompanied by a corresponding increase in sympathetic nerve activity. The magnitude of the pressor response was again larger in the DOCA than in the SHAM rats. Spinal section abolished the initial depressor phase but did not much affect the sustained pressor phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Centrally induced vasopressor and sympathetic nerve responses to carbachol in rats.

Blood pressure rose when carbachol was injected into the cerebral ventricles in conscious rats, but the heart rate fell. When rats were later anesthetized with urethane to allow recording of abdominal sympathetic nerve activity, carbachol injected similarly produced the following biphasic responses: initial vasodepression followed by a sustained pressor phase accompanied by corresponding changes in peripheral sympathetic nerve activity. The heart rate was transiently suppressed following the injection. Spinal section abolished the initial hypotensive phase and accompanying bradycardia and made the response purely pressor. By contrast, intravenous injections elicited purely vasodepressor responses. Thus, carbachol administered centrally caused vasopressor responses possibly via both activation of sympathetic vasomotor centers and a release of pituitary hormones. Since anesthesia attenuated the pressor responses and made them biphasic, these results indicate that central cholinergic mechanisms are inhibited during anesthesia and that a sympatho-inhibitory mechanism of cholinergic receptors exists behind the pressor responses, as disclosed during anesthesia.

Influence of ischemia and hypoxia on breathing in ducks.

We examined the influence of whole and lower body hypoxia and lower body ischemia on breathing in White Pekin ducks, Anas platyrhynchos, excluding pathways involving the carotid bodies. Carotid body denervated birds breathing 10 or 5% O2 developed a tachypnea after a latency of 30-100 s. The tachypnea was more pronounced with the more severe hypoxia, resulting in almost a doubling of minute ventilation (VE). Occlusion of the abdominal aorta in unanesthetized ducks produced immediate development of hypertension. Ventilation was unaffected for the 1st min; a tachypnea then developed rapidly and persisted for the duration of the occlusion resulting in a 25% increase in VE. After thoracic spinal section, all ventilatory responses to occlusion were eliminated. Experimental perfusion of the brain and single intact carotid body in unanesthetized ducks with hyperoxic blood during low O2 breathing (6-9% O2) resulted in tachypnea, also after a considerable latency. These results suggest that severe hypoxia can affect breathing in birds via pathways other than those involving the carotid bodies.

Control of blood flow in the cat spinal cord.

Spinal cord blood flow (SCBF) and the effect of end-tidal CO2 concentration (ETCO2) on SCBF (CO2 reactivity) were studied in the lumbar spinal cord of cats by means of the hydrogen-clearance technique Hydrogen gas was administered by inhalation, and its level in spinal cord tissue was estimated amperometrically with small (75 micrometers) platinum electrodes. The average SCBF's at normocapnia (ETCO2 = 4%) of the ventral horn gray matter and of the white matter at several locations were 43.2 and 16.2 ml . 100 gm-1 . min-1, respectively. For gray and white matter, the values of CO2 reactivity, estimated by the coefficient of the regression of SCBF (ml . 100 gm-1 . min-1) on ETCO2 (ml . 100 ml-1) were 11.6 and 2.1, respectively. No differences in SCBF or CO2 reactivity were observed between intact animals kept under N2O-O2 ventilation and decerebrated animals with no anesthesia. After an acute spinal section, ventral horn SCBF and CO2 reactivity (measured eight segments below the cordotomy) were not altered, in spite of the profound neural depression present (that is, spinal shock). Orthodromic (dorsal root) stimulation of the ventral horn neurons induced an average increase in blood flow of 128% above control values. Antidromic (ventral root) motoneuron activation failed to produce any significant changes in ventral horn blood flow.

The role of the sympathetic nervous system in congestive heart failure.

Congestive heart failure is usually accompanied by cardiovascular signs of an increased sympathetic and a decreased parasympathetic efferent activity. A current hypothesis for these autonomic changes holds the baroreceptor mechanisms mainly responsible for this complex neural reflex pattern together with a decreased responsiveness of cardiac vagal afferent ffibers. An alternative hypothesis is proposed here. Afferent sympathetic fibers with sensory endings in the atria and in the pulmonary veins are progressively excited by volume load. In cats with a chronic spinal section at C8, breathing spontaneously, an infusion of saline induces a reflex tachycardia through a sympatho-sympathetic neural circuit. In chronic dogs with intact cardiovascular innervation, the stimulation of aortic or cardiac sympathetic afferent fibers elicits an excitatory sympathetic reflex leading to hypertension and tachycardia; in addition, the sensitivity of baroreflexes is markedly reduced. Therefore, in congestive heart failure, especially in the absence of hypotension, the reflex excitation of the sympathetic outflow and the inhibition of the vagal efferent activity directed to the heart could be due to reflex mechanisms mediated by sympathetic cardiovascular afferents.

Effects of local anesthesia on persistence of peripherally induced postural asymmetries in rats.

Hindlimb flexion induced by direct stimulation of the hindlimb has been observed subsequent to spinal section if an appropriate time interval was allowed to elapse between onset of flexion and spinal cord section. The present series of experiments was conducted to test the possibility that asymmetry persistence is a product of ongoing cutaneous input that continues after stimulation offset and spinal cord section. A local anesthetic (lidocaine) was injected in the general area of stimulation, and its effects on asymmetry were assessed in three experiments. The results generally indicated that ongoing cutaneous input was not a sufficient explanation for persistence of flexion in animals stimulated with intact or severed spinal cords. The data revealed, however, that ongoing cutaneous input may partially explain results of a previous study that employed a "stimulation-wait" preparation to obtain peripherally induced spinal fixation.

Effects of manipulating stimulation intensity and duration on fixation of a peripherally-induced spinal reflex alteration in rats

Two studies were conducted to examine the effects of manipulating stimulation intensity and duration on post-spinal-section retention of a peripherally induced postural asymmetry. In the first experiment, two groups of rats received 1–3 mA of hindlimb stimulation for 60 or 90 min followed by a spinal cord section. Even though all animals demonstrated postsection persistence of asymmetry, significant differences between the two groups of animals were not discerned. Experiment 2 was conducted to more systematically evaluate intensity and duration manipulations. Twelve groups of rats that received 1, 3, or 5 mA of stimulation for either 30, 45, 60, or 90 min were used. Significant differences were found between intensity groups when presection asymmetry, postsection asymmetry, and percentage retention measures were analyzed. Significant differences between duration groups were found only when the 90 min groups were compared with animals that were given shorter periods of stimulation and when 60 min groups were compared to 30 min groups. From these data we have concluded that the intensity of the fixating stimulus is a major determinant of the magnitude of asymmetry persistence observed after spinal section.