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Excess dietary salt intake excites central sympathetic networks, which may be related to plasma hypernatremia. Plasma hypernatremia also occurs following water deprivation (WD). The purpose of this study was to test the hypothesis that WD induces hypernatremia and consequently augments sympathetic and pressor responses to sympathoexcitatory stimuli in rats and humans. Sympathetic nerve activity (SNA) and arterial blood pressure (ABP) responses to sciatic afferent nerve stimulation (2–20 Hz) and chemical stimulation of the rostral ventrolateral medulla (RVLM) were assessed in rats after 48 h of WD and compared with normally hydrated control rats (CON). In a parallel randomized-crossover human experiment ( n = 13 healthy young adults), sympathetic (microneurography) and pressor (photoplethysmography) responses to static exercise were compared between 16-h WD and CON conditions. In rats, plasma [Na+] was significantly higher in WD versus CON [136 ± 2 vs. 144 ± 2 (SD) mM, P < 0.01], but sciatic afferent nerve stimulation produced similar increases in renal SNA [5 Hz, 174 ± 34 vs. 169 ± 49% (SD), n = 6–8] and mean ABP [5 Hz, 21 ± 6 vs. 18 ± 7 (SD mmHg, n = 6–8]. RVLM injection of l-glutamate also produced similar increases in SNA and ABP in WD versus CON rats. In humans, WD increased serum [Na+] [140.6 ± 2.1 vs. 142.1 ± 1.9 mM (SD), P = 0.02] but did not augment sympathetic [muscle SNA: change from baseline (Δ) 6 ± 7 vs. 5 ± 7 (SD) bursts/min, P = 0.83] or mean ABP [Δ 12 ± 5 vs. 11 ± 8 (SD) mmHg, P = 0.73; WD vs. CON for all results] responses during the final minute of exercise. These findings suggest that despite eliciting relative hypernatremia, WD does not augment sympathetic or pressor responses to sciatic afferent stimulation in rats or to static exercise in humans. NEW & NOTEWORTHY Excess dietary salt intake excites central sympathetic networks, which may be related to plasma hypernatremia. Plasma hypernatremia also occurs following water deprivation (WD). We sought to determine whether plasma hypernatremia/hyperosmolality induced by WD augments sympathetic and pressor responses to sympathoexcitatory stimuli. Our findings suggest that WD does not augment sympathetic or pressor responses to sciatic afferent nerve stimulation in rats or to static exercise in humans.

Obstructive sleep apnea (OSA) is a disorder characterized by collapse of the velopharynx and/or oropharynx during sleep when drive to the upper airway is reduced. Here, we explore an indirect approach for activation of upper airway muscles that might affect airway dynamics, namely, unilateral electrical stimulation of the afferent fibers of the sciatic nerve, in an anesthetized rabbit model. A nerve cuff electrode was placed around the sciatic and hypoglossal nerves to deliver stimulus while airflow, air pressure, and alae nasi electromyogram (EMG) were monitored both before and after sciatic transection. Sciatic nerve stimulation increased respiratory effort, rate, and alae nasi EMG, which persisted for seconds after stimulation; however, upper airway resistance was unchanged. Hypoglossal stimulation reduced resistance without altering drive. Although sciatic nerve stimulation is not ideal for treating OSA, it remains a target for altering respiratory drive. NEW & NOTEWORTHY Previously, sciatic nerve stimulation has been shown to activate upper airway and chest wall muscles. The supposition that resistance through the upper airway would be reduced with this afferent reflex was disproven. Findings were in contrast with the effect of hypoglossal nerve stimulation, which was shown to decrease resistance without changing muscle activation or ventilatory drive.

The purpose of this study was to develop and implement a new technique for repeated monitoring of spinal mid- to long-latency somatosensory evoked potentials (SpSEPs) during sciatic nerve stimulation following recovery from spinal cord injury (SCI) in rats. Results of this study showed significant reproducibility of SpSEP components between specimens (analysis of variance [ANOVA], p0.05) and recording days (ANOVA, p0.700) using this technique. SpSEP amplitudes were significantly reduced (approximately 50% of uninjured amplitude, ANOVA, p0.001) following SCI and remained depressed for 10 weeks post-injury. SpSEP amplitude following high-intensity stimuli (1 mA) correlated with BBB locomotor score (Pearson, R0.353, P0.001). Characteristics of the mid- to long-latency SpSEPs suggest these components may reflect the integrity of the lateral pain pathway within the spinothalamic tract (STT). The technique and data presented in this study may be useful in future studies aimed at quantifying spinal cord integrity following injury and treatment using the rat model of SCI.

Objective We have previously reported that the measurement of spinal cord evoked magnetic fields (SCEFs) could be a helpful method for evaluating spinal cord function or detecting conduction blocks in the spinal cord. However, there have been no reports about segmental-SCEFs as a complex of axonal and synaptic activities in the spinal cord. The purpose of this study is to record and evaluate segmental-SCEFs. Methods The segmental-SCEFs were measured over the lumbar dural tubes of adult rabbits using our SQUID system following sciatic nerve stimulation; spinal cord evoked potentials (SCEPs) were also measured to compare the results. Results SCEPs showed conductive sharp waves following gentle waves, suggesting action potentials and synaptic potentials, respectively. The isomagnetic field maps of SCEFs showed a quadrupolar pattern propagating from the caudal to the cranial region within a short latency time, and after the conductive magnetic fields passed, stationary dipolar fields appeared and were sustained at some vertebral levels. Conclusions The quadrupolar magnetic fields were estimated to be generated from conducting action potentials, and the dipolar fields were thought to be caused by synaptic activities. Significance Through the measurement of segmental-SCEFs, the conductive neural and synaptic activities in the spinal cord can be visualized and distinguished. This is the first report to record and visualize the sequence of events ranging from the axonal activities of peripheral nerves and the spinal tract to the synaptic activities in the spinal cord.

In this study we hypothesized that reduced renal mass (RRM) hypertension, which is associated with a chronic reduction in vessel density, could reduce steady-state muscle performance. Vessel density and isometric tetanic force from the in situ gastrocnemius-plantaris-soleus muscle group were studied in age-matched normotensive sham-operated control (HSS) and hypertensive RRM rats on a high-salt (4.0% NaCl) diet (HSRRM) and a low-salt (0.4% NaCl) diet (LSS and LSRRM, respectively). The Achilles tendon was isolated and connected to a force transducer. Peak isometric tension elicited by sciatic nerve stimulation (1/s for 10 min, 50 impulses/s for 330 ms) was not different between the groups. In the LSS, HSS, and LSRRM groups, tension decreased similarly at 3 min to 375 +/- 22, 447 +/- 26, and 424 +/- 21 g/g, respectively. Tension was significantly reduced in the HSRRM group (203 +/- 45 g/g) relative to the LSS, HSS, and LSRRM groups by 3 min. These differences in steady-state tension persisted throughout the remainder of the experiment. Microvessel density, measured by the lectin fluorescence technique, was reduced significantly only in the soleus, plantaris, and medial gastrocnemius of the HSRRM rats. We conclude that RRM hypertension results in reductions in vessel density (rarefaction) that are associated with decreased steady-state muscle performance.

We simultaneously measured pial arteriolar diameter and changes in cortical blood flow during activation of the somatosensory cortex by sciatic nerve stimulation. The pial vasculature was visualized with a closed-cranial window technique in chloralose-anesthetized rats ( n = 13). Local blood flow was monitored with laser-Doppler flowmetry. During stimulation of the sciatic nerve (0.2 V, 5 Hz, 20 s), vascular diameter and laser-Doppler flow consistently displayed similar response profiles. With 0.5-ms stimulation pulses, the responses showed an initial peak followed by a smaller but sustained plateau dilation. In contrast, 5-ms pulses evoked a monotonically rising response. Our results support the concept that pial arteriolar diameter changes reflect cortical blood flow responses during somatosensory stimulation.

Focal spinal cord blood flow was measured in the left dorsal column during left sciatic nerve stimulation, and compared to blood flow in the same area during sciatic nerve inactivity. Blood flow was found to be significantly increased during stimulation. It is suggested that this increased blood flow is a reflection of increased metabolic demands of the neurons and synaptic systems within the internuncial neural pools, activated by stimulation of all components of the sciatic nerve, rather than a reflection of increased non-synaptic axonal conduction in the dorsal column.

Studies from this laboratory have demonstrated that the adrenocortical response following sciatic nerve stimulation is completely inhibited in rats with hypothalamic islands, indicating that this response depends entirely on the activation of afferent neural pathways to the hypothalamus. With the purpose of identifying the site of entry of these neural pathways into the mediobasal hypothalamus the effects of partial hypothalamic deafferentations were studied. It was found that in rats with posterior or posterolateral deafferentation the adrenocortical responses were similar to those obtained in intact rats, while anterior and anterolateral deafferentation resulted in a reduction of 62.3 and 53.3 %, respectively. These results would indicate that the sciatic impulses which activate the adrenocortical response involve neural afferents which enter the mediobasal hypothalamus by an anterior pathway.

Experimental evidence for the release of prostaglandin-like substances, mainly of the E type, into the venous outflow from working skeletal muscles in the dog is described. Muscular exercise of the hind-leg produced by sciatic nerve stimulation evoked the release of prostaglandin-like substances detected in femoral venous blood by the bioassay method. This release occurred during and after muscular work, was abolished by indomethacin, and was not present in gallamine-treated dogs. The results suggest that endogenous vasodilator prostaglandins released during and after muscular work may contribute to local hyperaemic response during and, mainly, after muscular activity.

Spontaneous and evoked hypothalamic unit activity in response to sensory stimuli was studied in acute experiments on anesthetized kittens. After the second day of postnatal development, spontaneous unit activity can be recorded in the posterior hypothalamus. Evoked responses to sciatic nerve stimulation were recorded on the fourth to fifth day after birth. In the early stages of development phasic and tonic types of unit responses are present in the hypothalamus, with some predominance of phasic. At the end of the third week responses of hypothalamic neurons in kittens have still not reached their definitive formation.

Previous studies from this laboratory have demonstrated that in rats with hypothalamic islands the adrenocortical response to photic and acoustic stimulation was partially inhibited indicating that they were at least to a certain degree neurally mediated, though ether stress produced normal adrenocortical responses. With the purpose of determining to what extent afferent somatosensory connections to the hypothalamus participate in the activation of adrenocortical responses following sciatic nerve stimulation, the effects of this stimulus applied through chronically implanted electrodes were studied on the plasma corticosterone levels in pentobarbital anaesthetized intact animals and in rats with hypothalamic islands. Ether stress or sciatic nerve stimulation for 2 min in intact rats produced a rise of plasma corticosterone to 32.1 plus or minus 1.2 and 32.1 plus or minus 1.8 mug/100 ml, respectively. However, in animals with hypothalamic islands the corresponding values were 29.2 plus or minus 1.8 and 12.4 plus or minus 0.8 mug/100 ml, respectively. The latter value was not significantly different from the basal corticosterone levels (13.0 plus or minus 1.2 mug/100 ml) found in rats 15 min after pentobarbital anaesthesia, the time when the sciatic stimulus was applied. The present data indicate that the adrenocortical discharge following sciatic nerve stimulation is completely inhibited by hypothalamic deafferentation and therefore depends entirely on the activation of the afferent neural pathways to the hypothalamus.

Prolonged changes in single-cell activity in the lateral geniculate nucleus are produced by sciatic nerve stimulation in anesthetized cats. The increases or decreases in activity may last for several minutes. Interval histograms show that the changes occur primarily in the short-interval distribution. Changes in single- and multi-unit records obtained simultaneously are usually, but not always, positively correlated. The possible mechanisms and implications of the prolonged changes are discussed.

Staphylococcal alpha-hemolysin injected iv into rabbits causes disappearance of the brain bioelectric activity, with particular involvement of the thalamic region. The toxin produces disintegration of the electronegative component of evoked potentials produced by sciatic nerve stimulation. It is postulated that alpha-hemolysin acts on both specific and nonspecific thalamic structures. Observed differences concern only the sequence of action on individual parts of the afferent system.

The evoked responses observed in the parietal associative zone are made up of two components with a short (ECAR) and a long latency (LCAR). The messages at the origin of the short latency waves and the localization of the activated cells were investigated, mainly during somatic stimulation. Animals anaesthetized with Nembutal were mainly used; some animals under chloralose and some under local analgesia were used for comparison. 1. 1. In the case of animals anaesthetized with Nembutal, only ECAR were recorded, while ECAR and LCAR appeared in animals under local analgesia or chloralose. 2. 2. ECARs evoked by sciatic nerve stimulation were essentially negative, those evoked by brachial nerve stimulation were diphasic (positive-negative), the negativity being greater. The latencies of these responses were the same as those of evoked potentials in the respective primary areas of projection. 3. 3. A series of experiments was made to demonstrate that ECARs appear independently of primary cortical evoked response (PR). A narrow zone of silence separates the regions in which each response can be recorded. ECARs can be recorded in conditions of depression when PR are absent. Reciprocal effects can be observed. Suppression of PR by local application of KCl and removal of primary projection areas did not affect ECARs. 4. 4. Records of deep cortical activities as well as transection of the thalamic cortical pathways have been made to demonstrate that ECARs are not due to diffusion from thalamic evoked activities. 5. 5. Disappearance of ECARs after local applications of KCl on the associative cortex, as well as micro-electrode recordings, show that the cells responsible for these short latency activities belong to the associative cortex. 6. 6. Disappearance of ECARs after coagulation of n. ventralis posterior and demonstration that this type of response has many of its characteristics in common with those from structures receiving specific afferents, lead to the conclusion that VP is the thalamic relay for the messages that provoke ECARs. 7. 7. The existence of a possible direct thalamocortical pathway, the type of synaptic junctions at the cortical level responsible for ECARs and the possible integrative role of these responses are discussed.

1. 1. Nerve-muscle function was studied at a variety of temperatures in the most northerly American frog, Rana sylvatica , and in a southern (west-central Mexico) population of Rana pipiens . 2. 2. Maximal twitch tension in isolated gastrocnemius muscles increased with decreasing temperature in R. sylvatica but decreased with decreasing temperature in R. pipiens . 3. 3. R. sylvatica muscles excitable to sciatic nerve stimulation until the freezing point (−3 to −5°C) was reached. Muscles from R. pipiens became inexcitable to either nerve or direct stimulation at about 0°C. 4. 4. No temperature-related differences in nerve function were seen between the two species.

Desipramine in intravenous doses of 0.3 to 3 mg/kg in the cat enhances preganglionic cervical sympathetic nerve activity evoked by hypothalamic stimulation. This effect is dependent on the pulse frequency of stimulation. Spontaneous potentials are in general slightly diminished. Reflex excitation of preganglionic sympathetic outflow induced by sciatic nerve stimulation is not altered by desipramine. The described effects are interpreted as the result of a modulating influence of desipramine on central structures controlling sympathetic outflow.

It has been known that a short-lasting stimulation of the somatic afferent nerves elicits either a depressor or a pressor response depending on the stimulus parameters (Johansson 1962). In the present study cardiovascular responses were observed during and after a long-lasting sciatic nerve stimulation in conscious spontaneously hypertensive rats (SHR) and their normotensive controls, the Wistar Kyoto rats (WKR).

Serum ACTH levels were determined by RIA following sciatic nerve stimulation, in intact rats and in rats bearing anterior (AHD), posterior (PHD) or complete (CHD) hypothalamic deafferentations. In both N and PHD groups, serum ACTH concentrations were markedly elevated following stimulation. In CHD animals this response was completely eliminated, and in the AHD group only a very slight and marginally significant increase in serum ACTH occurred, upon stimulation. These results demonstrate that the increased corticosterone secretion which occurs following sciatic nerve stimulation is due to elevated blood levels of ACTH, and confirm that this somatosensory stimulation impinges upon the hypothalamus from the rostral directions.

Neuroendocrine studies have demonstrated that photic, acoustic, and sciatic nerve stimulation produce adrenocortical discharges and these can be blocked by partial hypothalamic deafferentations and medial forebrain bundle (MFB) lesions. The effects of these sensory stimuli on single-cell activity of mediobasal hypothalamic (MBH) neurons were studied in intact male rats and in animals with anterior, anterolateral, and posterolateral hypothalamic deafferentations and bilateral MFB lesions. The data were analyzed as to changes in responsiveness, facilitation: inhibition ratio, patterns of firing, magnitude of response, frequency distribution, and sensory convergence. Photic projections enter the MBH both anteriorly and posteriorly and via the MFB, acoustic afferent fibers utilize the MFB, and the sciatic impulses arrive posteriorly. The MFB has also an inhibitory modulation on the photic, acoustic, and sciatic responses and AHD has the same effect on the latter. MFB lesions reduced most markedly the sensory convergence of the three modalities. The relation of these electrophysiologic findings to neuroendocrine studies on the neural pathways mediating adrenocortical responses are discussed.

In view of the possible role of serotonin in adrenocortical regulation, basal plasma corticosterone concentrations and the response to ether stress, photic, acoustic, or sciatic nerve stimulation, were studied in rats with 5,7-dihydroxytryptamine or vehicle injected into the raphe nuclei. The neurotoxin inhibited the response to photic stimulation without affecting the other modalities. This may suggest that the depletion of brain serotonin has a differential effect on the transmission of neural impulses which activate the adrenal cortex.

In order to evaluate the relationship between locus coeruleus (LC) spontaneous activity and LC activity in response to sensory stimuli, the effects of carbachol on both types of LC neuronal activity were investigated in anesthetized rats. Carbachol increased LC spontaneous discharge rate and altered the pattern of LC discharge in response to sciatic nerve stimulation, while saline had no effect. Moreover, the magnitudes of increases in LC spontaneous discharge rate produced by carbachol were highly correlated ( r =0.79) with a measure of simultaneous effects on LC sensory responses. These results suggest that drugs which increase LC spontaneous activity will also disrupt the pattern of LC discharge to sensory stimuli.

The response characteristics of interpositus neurones (IP) to sciatic nerve stimulation were studied in normal and Lurcher mutant mice under pentobarbitone anaesthesia. The response of IP neurones in the normal mouse was a short latency bimodal excitation (E1-I1-E2) followed by a depression of the firing rate (I2) and ending with a longer latency excitation (E3) which was completed within 225 msec. The response of the majority of IP neurones in the Lurcher mouse was a short latency unimodal excitation (LE1) which corresponded in time to the E1-I1-E2 phase in the normal. This was followed by a pause in the excitation. The response ended with a longer latency excitation (LE2) corresponding in time to the E3 phase in the normal mouse but which persisted for a considerably greater period of time. The response of IP neurones in normal and Lurcher mice appear to be similar to those observed in the normal and experimentally cerebellar decorticate cat, respectively.

Reflex responses in sympathetic efferent activity to electrical stimulation of somatic afferent nerves were investigated. The integrated reflex activity was expressed as a two-variable function of the stimulus intensity and frequency. It was determined that a fourth order polynomial describes the reflex activity with an error of less than 5%. The stimulus parameters were designed optimally to obtain maximum information of the process with a minimum of stimuli. Reflex activities of cardiac and peripheral vasomotor nerves evoked by sciatic nerve stimulation were analyzed with the method.

✓ Averaged somatosensory evoked potentials from the epidural space in response to sciatic nerve stimulation were recorded in bipolar and common reference mode in cats following various types of injury. An investigation was conducted on the development and properties of the spinal evoked response recorded from the center of the injury site, designated here as the “spinal cord evoked injury potential.” Typically it is a two-peak monophasic positive potential, approximately 40 msec in duration, with a slight negative afterwave. With increasing distance from the site of injury, its amplitude rapidly decreases, whereas latency remains constant. The common reference recording technique resulted in an earlier and better demonstration of the evoked injury potential, especially when it was transitory or incomplete. When impairment of conduction developed gradually, the evoked injury potential developed gradually too. In serial recordings along the spinal cord axis, the transition from a normal triphasic to a monophasic evoked injury potential allowed a precise localization of the lesion. These data suggest that the diagnostic value of intraoperative spinal cord monitoring may be increased by adopting a technique that incorporates several epidural recordings with a common reference recording technique. The spinal cord evoked injury potential seems to be a more sensitive indicator of spinal cord injury than the cortical evoked potential. The findings are discussed in the light of the presently developing spinal cord monitoring techniques.

Russian investigators have recently reported clinical recovery of enzyme treated, spinal cord transected rats. Using the exact protocols outlined by Matinian and Andreasian, we repeated a portion of their experiment using a Lidase preparation manufactured in the USSR. Animals were evaluated for return of bladder function, clinical evidence of hind limb motor function, cortical evoked response after sciatic nerve stimulation, and axonal transport of cortically injected tritiate proline by regenerated corticospinal axons. The only difference between treated and control animals was that the mean total body weight of the treated animals increased more than that of controls (p less than 0.05). No animal walked, had return of voluntary motor activity, showed cortical evoked response, or had evidence for transport of tritiated proline over regenerated corticospinal axons.

Changes in weight, arterial and peripheral venous pressures, and venous outflow were measured during levarterenol infusion and sciatic nerve stimulation in an isolated hindlimb with constant arterial inflow. Our results indicate that the weight loss which occurs during these procedures is caused by peripheral venous constriction, and that the loss of volume from the hindlimb is almost entirely from the intravascular compartment.

In unrestrained cats with, chronically implanted electrodes reflex discharges evoked by afferent sciatic nerve stimulation have been recorded from the cervical sympathetic nerve during wakefulness and during the two states of sleep.

Evoked potentials were recorded in the various septal nuclei of cats under chloralose anesthesia, following sciatic nerve stimulation, and four types of responses which had both short and long latencies, were demonstrated. During the penetration of the septum, changes in amplitude, the appearance of new waves and phase reversals were found. A series of experiments were performed to determine the pathways which mediate the long latency responses to the septum. These experiments, which included the recording of evoked potentials in the hypothalamus, the study of neuronal recovery cycles as well as hypothalamic stimulations and lesions, have suggested that the impulses arrive by polysynaptic pathways to the medial forebrain bundle and from there are propagated to the septum, thus confirming anatomical observations. The septum has an important function in behavioral, autonomic and endocrine mechanisms and the described somatosensory projections and their interaction with central inputs play undoubtedly an important role in its regulatory activities.

Unit activity of inferior collicular neurons in rats was evoked by stimulation with 2 kHz tones, and was analysed by poststimulation time histograms. The evoked activity became significantly different in about 30% of the cases when the tone was preceded by electrical stimulation of the sciatic nerve or by stimulation of the eye by light flashes. The latter stimulation usually evoked also theta activity in the hippocampal EEG.