Procedure for the decerebration of the rat

SAPRU, H. N. AND A. J. KRIEGER. Procedure for the decerebration of the rat. BRAIN. RES. BULL. 3(6) 675–679, 1978.—A procedure for the decerebration of the rat was devised. The internal and external carotid arteries were ligated under halothane anesthesia. A transection was made at the mid-collicular level of the brain and the transected forebrain was removed. The posterior communicating arteries were occluded by suction and oxidized cellulose was packed around these vessels. The cut surface of the brain was covered with oxidized cellulose and the cranial cavity was filled with cotton balls. Head-up tilt, carotid occlusion and sodium cyanide responses indicated that the orthostatic, baro-, and chemo- reflexes were intact in these preparations. The stability of the preparation (for at least 8–10 hr) and the integrity of these reflexes indicate that the decerebrate rat may be a suitable alternative for studies involving brain stem regulatory mechanisms in this species when it is desirable to avoid general anesthetics.     

The accuracy of subjective clinical assessments of the patellar reflex

Introduction: Measurement precision and accuracy of spinal reflexes plays an essential role in the clinical neurological examination. Reflexes are conventionally assessed either electromyographically or with rating scales. In this study we compared objective kinematic T‐reflex and subjective assessments of patellar reflexes in 15 normal healthy subjects. Methods: Randomized recordings of objectively quantified reflexes were rated by 24 medical students, 16 general practitioners, and 12 neurologists, using a visual analog scale and the NINDS and Mayo clinical reflex scales. Results: For all groups of raters, Spearman rank correlations showed that subjective ratings significantly correlated with change of knee angle (R² = 0.72–0.79, P < 0.001) and maximum T‐reflex amplitude (R² = 0.84–0.94, P < 0.001). Stepwise multiple regression analysis showed that all subjective rater groups relied most on the change of knee angle to assess the reflex. Conclusions: These findings show that subjective assessments of reflexes using reflex rating scales correlate strongly with biomechanical and electromyographic measures. Muscle Nerve, 2013     

Role of spinal α1-adrenergic mechanisms in the control of lower urinary tract in the rat

The role of spinal α₁-adrenergic mechanisms in the control of urinary bladder function was examined in urethane (1.2 g/kg s.c.) anesthetized and decerebrate unanesthetized female Sprague–Dawley rats (250–320 g). Bladder activity was recorded via a transurethral catheter during continuous infusion (0.21 ml/min) cystometrograms or under isovolumetric conditions. All drugs were administered intrathecally at the L₆-S₁ segmental level of spinal cord. During cystometrograms, 3 or 30 nmol of phenylephrine (α₁-adrenergic agonist) did not alter bladder activity; whereas 300 nmol increased the intercontraction interval by 98% and pressure threshold for inducing micturition by 115%, but did not change bladder contraction amplitude. A large dose of phenylephrine (3000 nmol) completely blocked reflex voiding and induced overflow incontinence at a high baseline pressure (mean: 33 cmH₂O; range: 28–42 cmH₂O). Under isovolumetric conditions, 3–30 nmol of phenylephrine abolished bladder activity for 22–45 min; whereas smaller doses (0.003–0.3 nmol) were inactive. Doxazosin (50 nmol), an α₁-adrenergic antagonist, decreased intercontraction intervals but did not change bladder contraction amplitude during cystometrograms. Under isovolumetric conditions this dose of doxazosin increased bladder contraction frequency and decreased bladder contraction amplitude. Smaller doses (5 or 25 nmol) of doxazosin did not alter bladder activity. These studies suggest that two types of spinal α₁-adrenergic mechanisms are involved in reflex bladder activity: (1) inhibitory control of the frequency of voiding reflexes presumably by regulating afferent processing in the spinal cord and (2) facilitatory modulation of the descending limb of the micturition reflex pathway.     

Serial recording of reflexes after feline spinal cord transection

Implanted nerve cuff and muscle electrodes were used to serially record reflexes after spinal cord transection in cat. Recording of reflexes, in response to both sensory nerve and to mixed motor and sensory nerve stimulation, was accomplished through 2 months after cord section. Serial recording of afferent and efferent nerve volleys was achieved as well. Serial reflex changes that follow cord transection are described. Reflex amplitude to sensory nerve stimulation increased in two phases. The first increase was noted between 1 and 4 days after cord transection; the second increase was recorded between 2 and 4 weeks. These observations suggest that at least two neuronal mechanisms with distinct temporal courses mediate the appearance of spinal hyperreflexia. The animal model described may be useful for further study of the neuronal mechanisms which underlie the hyperreflexia of spinal cord injury.     

Thermoregulatory responses of decerebrate and spinal cats

Cooling the spinal cord of the unanesthetized cat elicited shivering, piloerection, and vasoconstriction. A high-level decerebration abolished these effects. Lowering the decerebration to the level of the lower pons or medulla reinstated these responses to spinal cord cooling. In unanesthetized chronic spinal cats, cooling the spinal cord below the level of a T6 transection produced similar thermoregulatory effects limited to the hind limbs, although it was of less intensity and without piloerection. A high-level decerebration abolished shivering in the forelimbs to whole body cooling, while permitting shivering below the level of transection to spinal cord cooling. Lowering the level of decerebration to the lower pons or medulla reinstated shivering, vasoconstriction, and piloerection in the forelimbs. The data suggest that there is a region in the midbrain and upper pontine tegmentum which exerts tonic inhibition on lower regions in the lower pons, medulla, and spnal cord. When released from inhibition these lower regions are capable of facilitating thermoregulatory responses. Such an organization resolves contradictory reports on the abolition of thermoregulation after decerebration and answers the question of why spinal cord cooling produces shivering in spinal preparations but not in decerebrate preparations.     

Glucose utilization and reflex activity of the transected rat spinal cord

Spinal cord glucose utilization (SCGU) of gray and white matter was studied with the quantitative autoradiography [¹⁴C]2-deoxyglucose methodology, below and above a complete low thoracic transection. One day after transection, a generalized decrease in SCGU was observed in gray matter, particularly marked in the dorsal horn of the lumbar cord. A progressive increase in SCGU was observed thereafter. Values reached levels greater than those of non-transected controls by 2 and 4 weeks after the intervention in ventral horn of the lumbar cord, and ventral and dorsal horn of the cervical cord. A similar behavior of SCGU was observed in white matter of transected animals. The development of 17 lumbar reflex modalities was quantified between days 1 and 28 after spinal transection. The delay in emergence of these reflexes was related to their complexity. Correlation of reflex scores with SCGU was significant for all lumbar cord regions but linearity of this relationship was only observed in white matter. These results uncover a close relationship between SCGU and reflex activity of the spinal cord below a complete transection, particularly striking in white matter and suggests a role of the fasciculi proprii of the spinal cord in this phenomenon.     

Flexor reflex decreases during sympathetic stimulation in chronic human spinal cord injury

A better understanding of autonomic influence on motor reflex pathways in spinal cord injury is important to the clinical management of autonomic dysreflexia and spasticity in spinal cord injured patients. The purpose of this study was to examine the modulation of flexor reflex windup during episodes of induced sympathetic activity in chronic human spinal cord injury (SCI). We simultaneously measured peripheral vascular conductance and the windup of the flexor reflex in response to conditioning stimuli of electrocutaneous stimulation to the opposite leg and bladder percussion. Flexor reflexes were quantified using torque measurements of the response to a noxious electrical stimulus applied to the skin of the medial arch of the foot. Both bladder percussion and skin conditioning stimuli produced a reduction (43–67%) in the ankle and hip flexor torques (p < 0.05) of the flexor reflex. This reduction was accompanied by a simultaneous reduction in vascular conductance, measured using venous plethysmography, with a time course that matched the flexor reflex depression. While there was an overall attenuation of the flexor reflex, windup of the flexor reflex to repeated stimuli was maintained during periods of increased sympathetic activity. This paradoxical depression of flexor reflexes and minimal effect on windup is consistent with inhibition of afferent feedback within the superficial dorsal horn. The results of this study bring attention to the possible interaction of motor and sympathetic reflexes in SCI above and below the T5 spinal level, and have implications for clinicians in spasticity management and for researchers investigating motor reflexes post SCI.     

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.     

Coexistence of autonomic and somatic mechanisms in the pressor areas of medulla in cats.

The effects of electrical stimulation and microinjection of sodium glutamate (0.5 M) in the sympathetic pressor areas of the dorsal medulla (DM), ventrolateral medulla (VLM), and parvocellular nucleus (PVC) on the knee jerk, crossed extension, and evoked potential of the L5 ventral root produced by intermittent electrical stimulation were studied in 98 adult cats anesthetized with chloralose and urethane. During electrical and glutamate stimulation of these pressor areas, in addition to the rise of systemic arterial blood pressure marked inhibition of the spinal reflex was produced, indicating presence of neuronal perikarya responsible for these actions. Mild to moderate augmentation of spinal reflexes was also observed during brain stimulation but only in a few cases. The magnitude of the somatic effects among the pressor areas of the VLM, DM, and PVC subsequent to glutamate activation was about the same. Induced spinal reflex inhibition, independent from the baroreceptor and vagal influence, remained essentially unaltered after acute midcollicular decerebration. The inhibition was also observed in cats decerebellated 8-10 days in advance. The inhibition was not affected after bilateral electrolytic- or kainic-acid-induced lesions in the paramedian reticular nucleus (PRN). On the contrary, PRN-induced spinal reflex inhibition was attenuated after bilateral lesions in the DM or VLM. Data suggest that there coexists neuronal subpopulations in the VLM, DM, and PVC that can affect both the sympathetic pressor systems and 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.     

Somatic depressor reflexes: results of specific 'depressor' afferents' excitation or an epiphenomenon of general anesthesia and certain decerebrations?

In chloralose-urethane anesthetized cats and unanesthetized decerebrate cats graded electrical stimulation of the tibial nerve A-afferents was performed and the resulting changes in the tibial nerve compound action potentials, heart rate and systemic arterial pressure were recorded. Three subgroups of the tibial nerve A delta-afferents were distinguished and their excitability, conduction velocity and relation to the circulatory reflexes were characterized. Stimulation of the same A-afferents evoked only tachycardic reflexes in high-mesencephalic unanesthetized cats while both tachy- and bradycardic reflexes developed in anesthetized brain-intact cats. The volleys of A beta-afferents elicited depressor reflexes in 50% of anesthetized cats but were ineffective in the other anesthetized brain-intact cats and in all the unanesthetized decerebrate cats. In anesthetized cats, the volleys of two low-threshold subgroups of A delta-afferents evoked only depressor reflexes and volleys of high-threshold A delta-afferents evoked both depressor and pressor reflexes in dependence on the deepness of anesthesia. In unanesthetized cats, effects of A delta-stimulation depended on the level of decerebration, being exclusively pressor when the most high-threshold A delta-fibers were stimulated in high-mesencephalic cats, both pressor and depressor when only low-threshold subgroups of A delta-fibers were stimulated in these cats, and exclusively depressor in prebulbar cats. The dependence of the direction of reflex blood pressure changes on the level of decerebration and anesthesia is incompatible with the classical concept of the so-called somatic depressor afferents. Moreover, general anesthesia is shown to suppress and invert not only excitatory effects of spinal A-afferents' volleys on sympathetic vasoconstrictor and cardioaccelerator neurones but the inhibitory effects of these afferents' signals on the vagal cardioinhibitory neurones, too. Contrary to this concept, we regard the 'somatic depressor reflexes' and accompanying bradycardia not as a result of 'specific' afferents excitation, but as an epiphenomenon of general anesthesia and certain decerebrations. This hypothesis is founded: (1) on the results of electrophysiological investigations of somato-sympathetic and somato-vagal reflexes indicating the existence of parallel excitatory and inhibitory interneuronal pathways between the spinal afferents and sympathetic and vagal neurones; and (2) on the assumption of unequal sensitivity of these pathways to certain anesthetics.(ABSTRACT TRUNCATED AT 400 WORDS)     

Suppressive effect of vagal afferents on the activity of the trigeminal spinal neurons related to the jaw-opening reflex in rats: involvement of the endogenous opioid system

The purpose of the present study is to test the hypothesis that via the endogenous pain control system, vagal afferent input modulates the activity of the trigeminal spinal nucleus oralis (TSNO) related to the tooth pulp (TP)-evoked jaw-opening reflex (JOR). Extracellular single-unit recordings were made from 36 TSNO units responding to TP electrical stimulation with a constant temporal relationship to a digastric electromyogram (dEMG) signal in 26 pentobarbital-anesthetized rats. The activity of 36 TSNO neurons and the amplitude of the dEMG increased proportionally during 1.0–3.5 times the threshold for JOR. Some of these neurons (4 out of 5) were also excited by chemical stimulation (bradykinin, 1–2 μl, 1 mM) of TP. In 31 out of 36 TSNO neurons (86%), their activities during tooth pulp stimulation were suppressed by conditioning stimulation of the right vagus nerve. The suppressive effect of vagal afferent stimulation occurred at conditioning-test intervals of 20–150 ms after the onset of the stimulation, and its maximal suppressive effect occurred at approximately 50 ms. The mean time course of this suppressive effect paralleled that of the dEMG. After administration of naloxone (0.5 and 1.0 mg/kg, i.v.), an opiate receptor blocker, the suppressive effect on the activity of TSNO neurons (6 out of 8) was significantly attenuated at the conditioning-test interval of 50 ms compared to the control (p < 0.01). These results suggested that vagal afferent input inhibits nociceptive transmission in the TSNO related to TP-evoked JOR and this inhibitory effect may occur via the endogenous opioid system in rats.     

Motoneuron membrane changes associated with spinal shock and the Schiff-Sherrington phenomenon

Following transection of the thoracic spinal cord, in a decerebrate cat, the forelimbs exhibit an enhanced extensor stretch reflex while the ipsilateral flexion reflex is more difficult to elicit (Schiff-Sherrington Phenomenon). The hindlimbs on the other hand have an increased threshold for the extensor stretch reflex while flexion reflexes are hyperactive (spinal shock). This investigation was designed to examine the synaptic events mediating the Schiff-Sherrington Phenomenon (SSP) and spinal shock; and to characterize any differences in the response of flexor and extensor α-motoneurons. This was accomplished by measuring membrane potential and input resistance of identified forelimb and hindlimb α-motoneurons before, during, and after coldblock of the low thoracic cord.During post-brachial spinal cord coldblock, forelimb extensor motoneurons depolarized while flexor motoneurons hyperpolarized. Both flexor and extensor motoneurons in the lumbar cord hyperpolarized. These observations account at least in part for the behavioral manifestation of increased extensor tone seen during the SSP and for the reflex depression seen during spinal shock.The membrane potential changes observed in this study were mediated through a direct effect on α-motoneurons since these animals were flaxedilized and gamma loop activity was probably negligible. The hyperpolarization of hindlimb motoneurons was apparently due to the removal of descending facilitation, while the depolarization seen in forelimb extensor motoneurons appeared to be due to a release of facilitation. The mechanism of the hyperpolarization observed in some forelimb motoneurons was unclear.     

Spinalization unmasks clonidine's alpha 1-adrenergic mediated excitation of the flexor reflex in rats

Clonidine exerts alpha 2-adrenergic mediated depressant effects on most behaviors measured in a normal animal. However, in the spinal-transected (spinalized) animal, clonidine apparently facilitates the flexor reflex through a stimulation of spinal alpha 1-adrenoceptors. The purpose of the present study was to determine if spinalization per se causes the shift in clonidine's profile from an alpha 2- to an alpha 1-adrenergic agonist. The hindlimb flexor reflex was elicited by electrical pulses delivered through electrodes implanted subcutaneously in the hindpaw and was measured with a force transducer and polygraph. In contrast to an alpha 2-adrenergic mediated inhibition of the flexor reflex in intact rats, clonidine produced an alpha 1-adrenergic mediated increase in flexor reflex amplitude in spinalized rats. Because decerebration did not alter the depression due to clonidine, and intraventricular (but not intrathecal) administration of oxymetazoline mimicked the effect of clonidine, the depressant effects of alpha 2-adrenergic agonists are mediated through alpha 2-adrenergic receptors localized in the brainstem. Alternate methods for inducing a functional spinal transection (spinal block with intrathecal procaine; spinal ligation) indicated that the shift in clonidine's effect from inhibition of the flexor reflex to excitation occurred immediately following spinalization. Spinal ligation did not produce alpha 1-adrenergic supersensitivity at 15 min or 2 hr after transection, as measured by alterations in [3H]prazosin receptor binding or behavioral responses to clonidine. Thus, the shift in clonidine's effects from alpha 2-adrenergic mediated inhibition of the flexor reflex in intact rats to alpha 1-adrenergic mediated excitation in spinalized rats results because spinal transection unmasks clonidine's alpha 1-adrenergic stimulatory effect. Other conditions under which clonidine exerts alpha 1-adrenoceptor mediated excitatory effects on behavior are discussed.     

Gait Analysis of Adult Paraplegic Rats after Spinal Cord Repair

This study presents a novel detailed method of analysis of rat gait and uses this method to demonstrate recovery of forward locomotion patterns in adult rats made paraplegic by surgical spinal cord transection and subjected to a novel strategy for spinal cord repair. Six normal rats were compared to five animals in which the cord was transected at T8–T9, and a 5-mm segment of the spinal cord removed, and to seven animals in which, following spinal cord transection and removal of a spinal cord segment, multiple intercostal peripheral nerve bridges were implanted, rerouting pathways from white to gray matter in both directions. The implanted area was filled with fibrin glue containing acidic fibroblast growth factor. Details of the repair strategy have been published (H. Cheng, Y. Cao, and L. Olson, 1996,Science273:510–513). Gait analysis was carried out 3 and 4 months after surgery and once in the normal animals. Animals were allowed to walk across a runway with a transparent floor. Each test consisted of five trials, and each trial was videorecorded from underneath. Using frame-by-frame playback, individual footprints were then recorded regarding location and order of limb use, as well as step quality (degree of weight bearing, etc.). These data allowed measuring runway transit time, five different measures of step numbers, all possible temporal patterns of limb use, stride length, and base of support. Transected controls remained paralyzed in the hindlimbs with only occasional reflex hindlimb movements without weight bearing. Animals subjected to the full repair procedure were significantly faster than the controls, used their hindlimbs for 25–30% of the movements, and regained several of the specific limb recruitment patterns used by normal rats. Taken together, the gait analysis data demonstrate remarkable recovery of coordinated gait in the repaired animals, which was significantly better than controls for all relevant parameters, while at the same time clearly inferior to normal rats for most of the examined parameters. We conclude that normal rats use a multitude of interchangeable step sequence patterns, and that our spinal cord repair strategy leads to recovery of some of these patterns following complete spinal cord transection. These data suggest functionally relevant neuronal communication across the lesion.     

Properties of the descending limb of the spinobulbospinal micturition reflex pathway in the cat

The micturition reflex is thought to be mediated by a spinobulbospinal reflex pathway passing through the rostral pons. This study examined the properties of the descending limb of the reflex pathway by monitoring the responses of the lower urinary tract to stimulation of the pons in the decerebrate cat. Electrical stimulation (300 μs pulses at 50 Hz intratrain frequencies, 300–500 ms trains, 0.5–15 V) in the region of the locus coeruleus (P 0.5–3.1/L 2–4/H to −2.75) was used to activate the descending excitatory pathway to the sacral parasympathetic nucleus. Low intensity stimulation induced small amplitude, short duration (14 ± 11cm H₂O, 10 ± 3s) bladder contractions in a partially full bladder, whereas higher intensity stimulation induced large amplitude, long duration (69 ± 29cm H₂O, 70 ± 44s) contractions which were similar to distension-induced reflex micturition contractions. The evoked bladder contractions coincided with a reduction in external urethral sphincter (EUS) EMG activity. Following bilateral L₇-S₃ dorsal root transection, electrical stimulation of the pons still elicited the small amplitude bladder contractions, but the larger amplitude, long duration micturition contractions were abolished. During these small evoked bladder contractions, a suppression of EUS activity still occurred following deafferentation, indicating a pontine mediated bladder/EUS synergy. It is concluded that the pons can initiate bladder contractions and coordinated bladder-sphincter activity, but that afferent feedback (via the dorsal roots) is needed to maintain the large amplitude micturition contractions.     

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.     

Somatovesical and vesicovesical excitatory reflexes in urethane-anaesthetized rats

The effect of spinal cord transection on excitatory somato- and vesicovesical micturition reflexes have been investigated in urethane-anaesthetized rats. In adult rats, 3 distinct types of excitatory reflexes to the bladder may be observed: a somatovesical reflex organized at spinal level and two vesicovesical reflexes organized at spinal and supraspinal level, respectively. In agreement with results of lesion experiments (Neurosci. Lett., 8 (1978) 27-33), bladder voiding is abolished following spinal cord transection although both somato- and vesicovesical reflexes may be demonstrated in acute spinal rats. Occurrence of the spinal vesicovesical reflex during the collecting phase of the cystometrogram appears to be inhibited by a supraspinal inhibitory pathway.     

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.     

The effects of decerebration and destruction of nucleus raphe magnus, periaqueductal grey matter and brainstem lateral reticular formation on the depression due to surgical trauma of the jaw-opening reflex evoked by tooth-pulp stimulation in the cat

The effects on the jaw-opening reflex evoked by tooth-pulp stimulation of surgical trauma, decerebration and the destruction of a number of nuclei associated with descending inhibition of trigeminal or spinal neurones have been investigated in the cat. Surgical preparation caused a progressive elevation of the digastric reflex threshold. After decerebration, reflex thresholds remained elevated for 8–11 h before returning to close to pre-surgical control values. Destruction of the nucleus raphe magnus and of the periaqueductal grey matter did not affect the depressed reflex in decerebrate or anaesthetized cats. Variable effects were produced by bilateral ablation of the juxta-raphe reticular formation and destruction of the rostral ipsilateral lateral reticular formation of the brainstem.