Search

In the present study, the extent to which the early component of somatosensory evoked potentials (SEPs) and the Hoffmann (H-) reflex induced by stimulation of the posterior tibial nerve are altered during the ascending and descending phases of fast plantarflexion was investigated. SEPSs and H-reflex of the soleus following tibial nerve stimulation were examined during fast plantarflexion when performed by nine normal subjects. The analyses focused on differences in amplitude modulation of the P30-P40 component of SEP and the H-reflex between the ascending and descending phases of full wave rectified and averaged soleus electromyographic (EMG) activity. The H-reflex amplitude was significantly increased and decreased during the ascending and descending phases more than under resting control conditions, respectively. The reduction of SEP amplitude was 49% for the ascending phase and 83% for the descending phases with respect to the resting situation. Modulation of SEP during the ascending and descending phases was robustly retained even during ischemic nerve blockade of large diameter afferent fibers. These findings suggest that the transmission of afferent inputs from muscle spindles to motoneurons and to the somatosensory cortex during fast isometric contraction of the plantar flexor is regulated in a time-dependent fashion by descending commands.

The purposes of this study were to investigate the effects of circumferential pressure on flexor carpi radialis (FCR) H-reflex in subjects without neuromuscular deficits and to evaluate the skin's contribution to this effect. FCR H-reflex was assessed in 43 subjects by measuring the peak-to-peak amplitude change before, during, and after circumferential pressure was applied to the forearm. Twelve H-reflexes (H/M ratio: M = 25%, SD = 14) were recorded before pressure application to obtain a baseline value ([H.sub.baseline]) to which all data were compared. A pneumatic 15 to 20-cm air splint inflated to 51-60 mmHg provided the pressure around the forearm. H-reflex recordings were taken at 1, 3, and 5 min. during ([H.sub.pressure]) and after pressure application. A second smaller study (placebo), in which the air splint was inflated to 0 mmHg, was conducted in 5 subjects to ensure that changes in reflex amplitudes were not a result of cutaneous effects. Two types of responses were observed in the FCR H-reflex following pressure application. One group of subjects significantly increased in H-reflex amplitude while another group decreased in H-reflex amplitude when compared to [H.sub.baseline]. Regression analysis found that [H.sub.max] explained 37.2% of the variance when controlling for [H.sub.baseline]. Subjects with larger [H.sub.max] showed an increase in [H.sub.pressure] while subjects with lower [H.sub.max] showed decreases in [H.sub.pressure]. The placebo study revealed no differences in H-reflex amplitude from baseline values, implying that skin stimulation from the air splint has no role in the effects observed. The dichotomous result indicates that pressure influences the upper extremity differently than it does the lower extremity in certain individuals. Clinicians, using circumferential pressure as a therapeutic modality to lower muscle activity of the upper extremity, need to be cognizant that pressure may have contrasting effects on their patients.

It has long been known that the esophageal distension produced by swallowing elicits a powerful proximal gastric relaxation. Gastroinhibitory control by the esophagus involves neural pathways from esophageal distension-sensitive neurons in the nucleus tractus solitarius centralis (cNTS) with connections to virtually all levels of the dorsal motor nucleus of the vagus (DMV). We have shown recently that cNTS responses are excitatory and primarily involve tyrosine hydroxylase-immunoreactive cells, whereas the DMV response involves both an [[alpha].sub.1] excitatory and an [[alpha].sub.2] inhibitory response. In the present study, using an esophageal balloon distension to evoke gastric relaxation (esophageal-gastric reflex, EGR), we investigated the peripheral pharmacological basis responsible for this reflex. Systemic administration of atropine methyl nitrate reduced the amplitude of the gastric relaxation to 52.0 [+ or -] 4.4% of the original EGR, whereas [N.sup.G]-nitro-L-arginine methyl ester (L-NAME) reduced it to 26.3 [+ or -] 7.2% of the original EGR. Concomitant administration of atropine methyl nitrate and L-NAME reduced the amplitude of the gastric relaxation to 4.0 [+ or -] 2.5% of control. This reduction in the amplitude of induced EGR is quite comparable (4.3 [+ or -] 2.6%) to that seen when the animal was pretreated with the nicotinic ganglionic blocker hexamethonium. In the presence of bethanechol, the amplitude of the esophageal distension-induced gastric relaxation was increased to 177.0 [+ or -] 10.0% of control; administration of L-NAME reduced this amplitude to 19.9 [+ or -] 9.5%. Our data provide a clear demonstration that the gastroinhibitory control by the esophagus is mediated via a dual vagal innervation consisting of inhibitory nitrergic and excitatory cholinergic transmission. receptive relaxation reflex; nonadrenergic; noncholinergic; vagovagal reflex

ABSTRACT. From among the diverse meanings of stability, the one the author adopts here is that the effects of a perturbation are opposed, and therefore small effects remain small. Except [...]

We have examined dynamic stiffness at the human ankle using position perturbations which were designed to provide a wide-bandwidth input with low average velocity. A parallel-cascade, nonlinear system identification technique was used to separate overall stiffness into intrinsic and reflex components. Intrinsic stiffness was described by a linear, second-order system similar to that demonstrated previously. Reflex stiffness dynamics were more complex, comprising a delay, a unidirectional rate-sensitive element and then lowpass dynamics. Reflex mechanisms were found to be most important at frequencies of 5-10 Hz. The gain and dynamics of reflex stiffness varied strongly with the parameters of the perturbation, the gain decreasing as the mean velocity of the perturbation increased. Under some conditions, torques generated by reflex mechanisms were of the same magnitude as those from intrinsic mechanisms. it is concluded that reflex stiffness can be large enough to be important functionally, but that its effects will depend strongly upon the particular conditions. Index Terms - Biological motor systems, biomechanics, identification, nervous system, stretch reflexes.

An analysis of reflex choices based on biological conflict models has proved that instincts may yield strategic values by providing a behaved emotional response. Likewise, it was shown that loss of temper tend to benefit a player under asymmetric conditions by imposing a rational awareness to engage in irrational fights. Individuals who are amply aware of their reflex choices can rationally manipulate their instinctual behaviour to their advantage.

Analysis of pre- and postsynaptic recordings from glycinergic inhibitory interneurons and Mauthner cell shows that the specific weak interneurons do not produce postsynaptic responses in comparison to functional neurons that always generate inhibitory postsynaptic potential. Subsequent to eighth nerve tetanic stimuli, weak connections exhibit enhanced transmission, supporting long-term potentiation of inhibitory synapses. Weak junctions are crucial for expression of plasticity within a network.

Activation of the baroreceptors in anaesthetized rats without and with LVD through phenylephrine-induced arterial pressure increase helps study the impairment of baroreflexes during left ventricular dysfunction (LVD) arising from chronic myocardial infarction without congestive heart failure and the role of abnormal central neural mechanisms in causing the impairment. The baroreflex regulation of ventilatory, sympathetic and heart rate responses in rats with moderate LVD is defective, and an inverse relationship exists between baroreflex gains and infarct size. The reduced baroreflexes may arise from abnormal afferent pathways despite the contribution of central mechanisms to the defective barosympathetic reflex.

Experimental measurement of the time course of variations in the baroreceptor control of heart rate in chronically instrumented rats reveal a variation in the totality of the sigmoidal curve that defines the baroreceptor control of heart rate after tail suspension. All parameters except the gain of the reflex remain changed after 48 h of release of tail suspension. Transient changes in the heart rate were seen after the return to horizontal position.

Electromyographic activity recordings in 17 decerebrated cats show that pharyngeal mucosal mechanoreceptors activate a pharyngo-upper esophageal sphincter (UES) contractile reflex. Both pressure and touch activate the pharyngeal mucosa. Transfection of pharynogoesophageal and glossopharyngeal nerves or anesthesia of mucosa inhibit the pharyngo-UES reflex but have no effect on esophago-UES contractile reflex.

A study of the human blink modulation of 49 people, using air puffs and sound bursts to elicit eye blink reflexes, revealed that emotions alter the expression of attentional mechanisms in the modulation of the eye blink reflex. The specification of attention resources effected changes in blink amplitude across sensory modalities. However, when attention was focused on an aversive stimulus, an increase in general reflex facilitation occurred.

Studies of anesthetized cats aid analysis of the reflex response of cardiac sympathetic nerve activity (CSNA) during static triceps surae muscle contraction. A reflex originating from the contracting muscle activates the cardiac sympathetic outflow. Stimulation of muscle mechanoreceptors causes enhancement in CSNA when static contraction starts, resulting in further enhancement caused by a reflex from muscle metaboreceptors.

Dynamic exercise resets the open-loop stimulus relation of the carotid-baroreflex by shifting the baroreflex response curve to the level of systemic pressure. This response of the carotid baroreflex is maintained at the same level of effectiveness when at rest and during exercise, involving transient changes in arterial pressure. Reflex alterations in heart rate and mean arterial pressure permit efficient buffering of elevations in systemic blood pressure by shifting the operating point toward baroreflex threshold.

Liu, Jianmin, Yoshihiro Yamamoto, Bruce D. Schirmer, Robert A. Ross, and Ravinder K. Mittal. Evidence for a peripheral mechanism of esophagocrural diaphragm inhibitory reflex in cats. Am. J. Physiol. Gastrointest. Liver Physiol. 278: G281-G288, 2000.--The esophagogastric junction (EGJ) is guarded by two sphincters, a smooth muscle lower esophageal sphincter (LES) and a skeletal muscle crural diaphragm. These two sphincters relax simultaneously under certain physiological conditions, i.e., swallowing, belching, vomiting, transient LES relaxation, and esophageal distension. Esophageal distension-induced crural diaphragm relaxation is mediated through vagal afferents that are thought to exert inhibitory influence on the central mechanism (brain stem) of crural diaphragm contraction. We conducted studies in 10 cats to determine whether a mechanism of crural diaphragm relaxation was located at the level of the neuromuscular junction and/or muscle. Stimulation of the crural diaphragm neuromuscular junction through 1) the electrodes implanted in the muscle and 2) the bilateral phrenic nerve resulted in an increase in EGJ pressure. Nicotinic receptor blockade (pancuronium, 0.2 mg/kg) abolished the EGJ pressure increase caused by electrical stimulation of the neuromuscular junction. Esophageal distension and bolus-induced secondary esophageal peristalsis caused relaxation of the EGJ during the stimulation of the neuromuscular junction. Bilateral phrenicotomy and vagotomy had no influence on this relaxation. These data suggest the existence of a peripheral mechanism of crural diaphragm inhibition. This peripheral inhibitory mechanism may reside at the level of either the neuromuscular junction or the skeletal muscle. crural diaphragm relaxation; neuromuscular junction; transient lower esophageal sphincter relaxation