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Temporal Interference Stimulation (TIS) has garnered significant attention as a methodology for non-invasively stimulating deep neural targets with minimal off-target activation. While most studies have employed TIS for non-invasive deep brain stimulation, invasive peripheral nerve TIS remains largely unexplored. Conventional peripheral nerve neuromodulation has been researched extensively and has many demonstrated therapeutic applications; however, clinical translation is limited by the specificity of the stimulation protocols and the accuracy of the in-silico models. Consequently, this work investigates the feasibility and specificity of invasive peripheral nerve TIS using a biophysical computational model of a human sciatic nerve and a multi-cuff electrode stimulator. First, an in-silico study of individual alpha motor neuron responses to TIS is conducted, which explores the optimality and relationships among an axon’s geometrical parameters, the stimulation frequencies, and the extracellular voltage distribution along the axon. It is demonstrated that static stimulation thresholds are ineffective for predicting motor neuron TIS responses and that TIS optimization methods developed for deep brain stimulation applications are not optimal for peripheral nerve stimulation. Second, a novel optimization methodology is proposed that projects a spatial stimulation waveform along a target axon in the nerve. It is shown that certain spatial distributions can reduce stimulation intensity in both the off-target and target regions, and thus, optimization of the spatial stimulation waveform can increase specificity. Third, multiple algorithm variations are compared using the sciatic nerve and cuff electrode computational model. Ultimately, the simulation results suggest that application-specific factors, e.g., the location of the target axon relative to the stimulation electrodes, dictate the optimal protocol parameters; however, the methodology presented in this dissertation can be used as a template for maximizing the specificity of a TIS protocol on a per-target basis.

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.

Objective Noninvasive and detailed visualization of electrophysiological activity in the thoracic spinal cord through magnetoneurography. Methods In five healthy volunteers, magnetic fields around current flowing in the thoracic spinal cord after alternating unilateral and synchronized bilateral sciatic nerve stimulation were measured using a magnetoneurograph system with superconductive quantum interference device biomagnetometers. The current distribution was obtained from the magnetic data by spatial filtering and visualized by superimposing it on the X-ray image. Conduction velocity was calculated using the peak latency of the current waveforms. Results A sufficiently high magnetic signal intensity and signal-to-noise ratio were obtained in all participants after synchronized bilateral sciatic nerve stimulation. Leading and trailing components along the spinal canal and inward components flowing into the depolarization site ascended to the upper thoracic spine. Conduction velocity of the inward current in the whole thoracic spine was 42.4 m/s. Conclusions Visualization of electrophysiological activity in the thoracic spinal cord was achieved through magnetoneurography and a new method for synchronized bilateral sciatic nerve stimulation. Magnetoneurography is expected to be a useful modality in functional assessment of thoracic myelopathy. Significance This is the first report to use magnetoneurography to noninvasively visualize electrophysiological activity in the thoracic spinal cord in detail.

Objective: To estimate the effectiveness of welding epineural coaptation of the residual sciatic nerve after resection based on electroneuromyographic (ENMG) parameters obtained in the gastrocnemius muscle. Materials and methods. Experimental animals were albino outbreed male rats (350–450 g, 7 months old); trauma model was the resection of the left sciatic nerve in the middle third; the experimental groups were as following: 1 — neurotomy (n = 18), 2 — neurotomy + neurosuture (n = 13), 3 — neurotomy + welding coaptation (n = 15); the method of investigation was direct needle ENMG (sciatic nerve stimulation, responses were registered in gastrocnemius muscle) in 3 and 5 months after injury. Results. The model of the nerve trauma with a temporary restriction of limb mobility is relevant for evaluating the effectiveness of restorative interventions in this type of pathology. In 5 months of observation there was found a significant prevalence of M-response amplitude in the injured limb compared to neurorrhaphy (17.3 ± 2.3 vs. 8.4 ± 0.9 mV, respectively; p = 0.005). M-response amplitude lateralization after the welded coaptation, in contrast to neurorrhaphy, is of temporary nature, indicating the improved regeneration process. Absence of ENMG-indices lateralization in 3 and 5 months after the neurotomy and high values of the M-response amplitude in 5 months indicated the possibility of gastrocnemius alternative re-innervations by terminals of intact nerve trunks. Conclusion. High-frequency electric epineural welding provides a reliable coaptation of the residual nerve, and, taking into account some ENMG indicators, is more effective than neurorrhaphy.

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.

Summary 1 The effect of pantoprazole on vecuronium-induced neuromuscular blockade in in vivo has not been clearly defined. In this study, we demonstrate that chronic administration, but not acute administration, of pantoprazole alters the pattern of vecuronium-induced neuromuscular blockade. 2 This study was designed to evaluate the effect of acute and chronic administration of pantoprazole on vecuronium-induced neuromuscular blockade using the rat in vivo sciatic nerve-stimulated gastrocnemius preparation. 3 Vecuronium was administered as a slow intravenous infusion (29.41 μg kg−1 min−1) until the gastrocnemius twitch response to sciatic nerve stimulation was completely abolished. The effect of acute (single dose, i.v.) and chronic administration (per oral for 21 days) of pantoprazole (3.64 mg kg−1) on vecuronium-induced blockade was assessed by comparing ED50 values, time required for 50% block, ED95 values, block duration and percentage of recovery with respect to control. 4 Acute administration of pantoprazole had no significant effect on any parameter of vecuronium-induced neuromuscular blockade. Chronic administration of pantoprazole significantly reduced vecuronium ED50 value, time for 50% block, ED95 value and percentage recovery from blockade compared with the control group (P

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.

Segmental-SCEFs of rabbits after sciatic nerve stimulation were detected by neuromagnetic recordings, and conductive neural activities and synaptic activities in the spinal cord were able to be visualized. The measurement of segmental-SCEFs could be a helpful method to evaluate the function of the spinal cord.

The electromyographic methods were performed to estimate the rat’s gastrocnemius muscle spinal motor center functional state under conditions of gravity unloading. The research was performed in the following experimental series: (1) after 35 days of microgravity influence; (2) after 35 days of microgravity influence in combination with support receptor excitation. The series of experiments showed that parameters of recorded evoked potentials in gastrocnemius muscle (GM) induced by sciatic nerve stimulation while gravity unloading (group 1), significantly differed from those registered in intact animals and not differed in group 2. It has been demonstrated that the reflex excitability of rat’s gastrocnemius muscle spinal motor center increases under conditions of gravity unloading. Support afferentation limitation plays the key role in motor centers state change.

In many functional neuroimaging research the change of local cerebral blood flow (CBF) induced by sensory stimulation is regarded as an indicator of the change in cortical neuronal activity although a precise and full spatio-temporal description of local CBF response coupled to neural activity has still not been laid out. Using the laser speckle imaging technique a relatively large exposed area in somatosensory cortex of rat was imaged for the observation of the variations of CBF during sciatic nerve stimulation. The results showed that cerebral blood flow activation was spatially localized and discretely distributed in the targeted microvasculature. Individual arteries, veins and capillaries in different diameters were activated with the time going. The response pattern of CBF related to the function of brainactivity and energy metabolism is delineated exactly.

Increases in the concentration of malonyl-CoA in skeletal muscle have been observed in the KKA(Y) mouse, an obese rodent with high plasma insulin and glucose levels. To assess whether insulin and glucose directly regulate malonyl-CoA in muscle, soleus muscles from young rats were incubated with insulin and glucose at various concentrations, and their content of malonyl-CoA was determined. In addition, the effect on malonyl-CoA of denervation and electrically-induced muscle contractions was assessed. The concentration of malonyl-CoA in the soleus, taken directly from a rat fed ad libitum, was 2.0 +/- 0.2 nmol/g. In muscles incubated for 20 min in a medium devoid of added insulin and glucose, the concentration was decreased to 0.8 +/- 0.2 nmol/g. When the medium contained 0.5, 7.5, or 30 mM glucose, malonyl-CoA concentrations were 1.3 +/- 0.1, 1.8 +/- 0.1, or 2.4 +/- 0.2 nmol/g, respectively, in the absence of insulin and 1.7 +/- 0.1, 4.6 +/- 0.3 and 5.5 +/- 0.6 nmol/g. in its presence (10 mU/ml). Compared with its level in a control muscle, the concentration of malonyl-CoA increased 3-fold in the soleus 6-8 h after denervation and remained 2-fold higher foror = 48 h. In contrast, muscle contractions induced by sciatic nerve stimulation, in vivo, acutely decreased the concentration of malonyl-CoA by 30-35%. The results indicate that insulin and glucose, and probably contractile activity, regulate the concentration of malonyl-CoA in muscle. They suggest that malonyl-CoA is a component of a fuel-sensing and signaling mechanism that responds to changes in the fuel milieu and possibly the energy expenditure of the muscle cell.

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.

The effect of a permanent magnetic field on evoked potentials in the cerebral and cerebellar cortex arising in response to sciatic nerve stimulation was investigated in experiments on rats. During exposure to a permanent magnetic field an increase in amplitude of the evoked potential was found and additional waves appeared in its structure. The effect increased with an increase in field intensity over the range 500–4000 Oe.

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.

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.

Opiate binding material (Fraction I and Fraction II) was observed to be released in vivo into the spinal superfusates of rats and cats under both resting and periods when either the hindpaw (rat) or sciatic nerve (cat) was stimulated. The release was stimulus-dependent and proportional to the frequency of stimulation.

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.

Publisher Summary This chapter demonstrates the inhibition of adrenocortical responses following sciatic nerve stimulation in rats with complete and partial hypothalamic deafferentation. The chapter indicates that the adrenocortical discharge following sciatic nerve stimulation is totally inhibited by complete hypothalamic deafferentation and that the afferent input is mediated by anterior neural pathways entering the hypothalamus. Partial hypothalamic deafferentation has demonstrated that the adrenocortical responses were inhibited following sciatic stimulation in rats with anterolateral and anterior cuts, however no such effects were obtained with posterior and posterolateral deafferentations. 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 plasma corticosterone levels in pentobarbital anesthetized intact animals and in rats with hypothalamic islands. In the same preparation anoxia, immobilization and ether-stress produced normal adrenocortical responses.

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.