Gastrin-releasing peptide is a modulatory neurotransmitter of the descending phase of the peristaltic reflex

The physiological role of gastrin-releasing peptide (GRP) and of its cognate receptors in regulating the intestinal peristaltic reflex was examined in a three-compartment flat-sheet preparation of rat colon. Mucosal stimulation applied to the central compartment at high, but not low levels of intensity, induced GRP release in the caudad compartment where descending relaxation was measured, but not into the ascending compartment where ascending contraction was measured or into the central compartment where the stimuli were applied. The selective GRP (BB(2)) receptor antagonist, [D-Phe(6),des-Met(14)]bombesin(6-14), inhibited descending relaxation and VIP release in the caudad compartment induced by high but not by low levels of stimulation applied to the mucosa in the central compartment. The selective neuromedin B (BB(1)) receptor antagonist, BIM-23127, had no effect on descending relaxation or VIP release. Neither the BB(1) nor the BB(2) antagonist had any effect on ascending contraction or substance P release in the orad compartment. Consistent with the effects of the antagonists on the peristaltic reflex, the BB(2) antagonist but not the BB(1) antagonist decreased the velocity of propulsion of artificial fecal pellets through isolated segments of guinea pig distal colon. The results indicate that GRP is selectively released from myenteric neurons in descending pathways during the peristaltic reflex and that it acts via BB(2) receptors to augment the descending phase of the peristaltic reflex and propulsion.     

Reciprocal activity of longitudinal and circular muscle during intestinal peristaltic reflex

A two-compartment, flat-sheet preparation of rat colon was devised, which enabled exclusive measurement of longitudinal muscle activity during the ascending and descending phases of the peristaltic reflex. A previous study using longitudinal muscle strips revealed the operation of an integrated neuronal circuit consisting of somatostatin, opioid, and VIP/pituitary adenylate cyclase-activating peptide (PACAP)/nitric oxide synthase (NOS) interneurons coupled to cholinergic/tachykinin motor neurons innervating longitudinal muscle strips that could lead to descending contraction and ascending relaxation of this muscle layer. Previous studies in peristaltic preparations have also shown that an increase in somatostatin release during the descending phase causes a decrease in Met-enkephalin release and suppression of the inhibitory effect of Met-enkephalin on VIP/PACAP/NOS motor neurons innervating circular muscle and a distinct set of VIP/PACAP/NOS interneurons. The present study showed that in contrast to circular muscle, longitudinal muscle contracted during the descending phase and relaxed during the ascending phase. Somatostatin antiserum inhibited descending contraction and augmented ascending relaxation of longitudinal muscle, whereas naloxone had the opposite effect. VIP and PACAP antagonists inhibited descending contraction of longitudinal muscle and augmented ascending relaxation. Atropine and tachykinin antagonists inhibited descending contraction of longitudinal muscle. As shown in earlier studies, the same antagonists and antisera produced opposite effects on circular muscle. We conclude that longitudinal muscle contracts and relaxes in reverse fashion to circular muscle during the peristaltic reflex. Longitudinal muscle activity is regulated by excitatory VIP/PACAP/NOS interneurons coupled to cholinergic/tachykinin motor neurons innervating longitudinal muscle.     

Physiological role of neuropeptide Y in the regulation of the ascending phase of the peristaltic reflex

The physiological role of neuropeptide Y (NPY) and of specific NPY receptors in regulating the intestinal peristaltic reflex was examined in three-compartment flat-sheet preparations of rat colon. Graded muscle stretch or mucosal stimulation applied to the central compartment inhibited NPY release in the orad compartment where ascending contraction was measured. NPY and the Y1-receptor agonist [Leu31, Pro34]NPY inhibited, whereas the selective Y1-receptor antagonist BIBP 3226 augmented ascending contraction and substance P (SP) release in the orad compartment induced by muscle stretch or mucosal stimulation. Neither agonist nor antagonist had any effect on descending relaxation or VIP release in the caudad compartment. The Y2-receptor agonist NPY13-36 and antagonist BIIE 0246 had no effect on peptide release or mechanical response. The results indicate that suppression of a tonic inhibitory influence of NPY neurons on excitatory neurotransmitter release contributes substantially to the orad contractile phase of the peristaltic reflex. The effect of NPY on neurotransmitter release is mediated by Y1 receptors.     

Adrenomedullary pressor responses to stimulation of the rostral hypothalamus in the rat: influence of adrenaline-induced vasodilation and reflex cardioinhibition

Electrical stimulation (100 Hz, 1 ms, 150 microA, 10 s) of the anterior hypothalamus in chloralose-anesthetized rats evoked a biphasic pressor response consisting of an initial sharp rise in arterial pressure at the onset of stimulation, followed by a second elevation after cessation of the stimulus. This response was accompanied by an increase in plasma noradrenaline and adrenaline levels. Peripheral sympathectomy with guanethidine selectively abolished the primary phase of the biphasic pressor response, while bilateral removal of the adrenal medulla eliminated only the secondary component. After alpha-adrenergic blockade with phentolamine, the primary phase of the stimulation-induced response was reduced while the secondary pressor component was blocked and replaced by a significant hypotension. The intravenous administration of sotalol enhanced the secondary pressor component without affecting the stimulation-induced plasma noradrenaline and adrenaline responses. After treatment with atropine, the secondary pressor effect was also potentiated, as the reflex bradycardia normally associated with the response was eliminated. A subsequent administration of sotalol in these rats further potentiated the secondary pressor component to stimulation. In rats treated with atropine and sotalol, the sympathetic vasomotor and the adrenomedullary pressor responses could be dissociated according to thresholds and stimulus frequency or current-response characteristics. The results suggest that in intact rats, adrenaline-induced vasodilation and reflex cardiac inhibition contribute to either reduce or mask the adrenomedullary component of the biphasic pressor response evoked by stimulation of the anterior hypothalamus. The study also raises the hypothesis of a dual regulation of both components of the sympathetic system in the anterior hypothalamic region.     

Functional coordination of motor activity in colonic smooth muscles in rat experimental model

Spontaneous and electrically-elicited motor activity was recorded by triple organ bath in rat segment-model preparation as display of excitation of local nerve networks and ascending or descending reflex pathways underlying contractile potency and functional coordination of colonic longitudinal and circular muscles. Spontaneous high-amplitude contractions, but not relaxations, appeared synchronously in both muscles. Electrical field stimulation applied to proximal or distal part of segments elicited both tetrodotoxin (0.1 microM)-sensitive local motor responses of the stimulated part and ascending or descending motor responses of the contralateral, nonstimulated part of the preparations. Contractions characterized the local response of longitudinal muscle. The circular muscle responded with relaxation followed by contraction. Synchronous ascending contractions and descending contraction of the longitudinal muscle and relaxation followed by contraction of the circular muscle were observed when the middle part of segments was stimulated, thus indicating that locally-induced nerve excitation propagated via intrinsic ascending or descending nerve pathways that could be synchronously coactivated by one and the same stimulus. The ascending motor responses were more pronounced and the motor responses of longitudinal muscle were expressed more than those of circular muscle suggesting an essential role of ascending reflex pathways and longitudinal muscle in the coordinated motor activity of colon.     

Mechanosensitive cardiac C-fiber response to changes in left ventricular filling, coronary perfusion pressure, hemorrhage, and volume expansion in rats

Left ventricular (LV) end-diastolic pressure (LVEDP) increase due to volume expansion (VExp) enhances mechanosensitive vagal cardiac afferent C-fiber activity (CNFA), thus decreasing renal sympathetic nerve activity (RSNA). Hypotensive hemorrhage (hHem) attenuates RSNA despite decreased LVEDP. We hypothesized that CNFA increases with any change in LVEDP. Coronary perfusion pressure (CPP), supposedly affected in both conditions, might also be a stimulus of CNFA. VExp and hHem were performed in anesthetized male Sprague-Dawley rats while blood pressure, heart rate, and RSNA were measured. Cervical vagotomy abolished RSNA response in both reflex responses. Single-unit CNFA was recorded while LVEDP was changed. Rapid changes (+/- 4, +/-6, +/-8 mmHg) were obtained by graded occlusion of the caval vein and descending aorta. Prolonged changes were obtained by VExp and hHem. Furthermore, CNFA was recorded in a modified Langendorff heart while CPP was changed (70, 100, 40 mmHg). Rapid LVEDP changes increased CNFA [caval vein occlusion: +16 +/- 3 Hz (approximately +602%); aortic occlusion: +15 +/- 3 Hz (approximately +553%); 70 units; P < 0.05]. VExp and hHem (n = 6) increased CNFA [VExp: +10 +/- 4 Hz (approximately +1,033%); hHem: +10 +/- 2 Hz (approximately +1,225%); P < 0.05]. An increase in CPP increased CNFA [+2 +/- 1 Hz (approximately +225%); P < 0.05], whereas a decrease in CPP decreased CNFA [-0.8 +/- 0.4 Hz (approximately -50%); P < 0.05]. All C fibers recorded originated from the LV. CNFA increased with any LVEDP change but changed equidirectionally with CPP. Thus neither LVEDP nor CPP fully accounts directly for afferent C-fiber and reflex sympathetic responses. The intrinsic afferent stimuli and receptive fields accounting for reflex sympathoinhibition still remain cryptic.     

Impaired gastrocolonic response and peristaltic reflex in slow-transit constipation: role of 5-HT(3) pathways

Colonic motility is modulated by the 5-hydroxytryptamine (5-HT)(3)-dependent gastrocolonic response and 5-HT(3)-independent peristaltic reflex. We compared descending colon tone responses to antral distension, duodenal lipid perfusion, and colonic distension after double-blind placebo or granisetron in 13 healthy volunteers and nine slow-transit constipated patients. Antral distension (100-300 ml) and duodenal lipids (3 kcal/min) evoked increases in colon tone in volunteers, which were blunted in constipated patients (P < 0.05). Granisetron (10 microg/kg) reduced responses to antral distension and lipids in volunteers and to lipids in constipated patients (P < 0.05). The ascending contraction of the peristaltic reflex was blunted in constipated patients (P < 0.05), whereas descending responses were similar. Granisetron did not modify the peristaltic reflex. Colonic responses to bethanechol were similar in patients and volunteers. In conclusion, antral distension- and duodenal lipid-activated gastrocolonic responses and ascending contractions of the peristaltic reflex are impaired with slow-transit constipation with loss of both 5-HT(3)-dependent and -independent function. Thus abnormalities of neural reflex modulation of colonic motor function may play pathophysiological roles in slow-transit constipation.     

Modulation of the baroreceptor reflex by the dorsomedial hypothalamic nucleus and perifornical area

Neurons within the dorsomedial hypothalamic nucleus (DMH) and perifornical area (PeF), which lie within the classic hypothalamic defense area, subserve the cardiovascular response to psychological stress. Previous studies have shown that electrical stimulation of the hypothalamic defense area causes inhibition of the cardiac and (in some cases) sympathetic components of the baroreceptor reflex. In contrast, naturally evoked psychological stress does not appear to be associated with such inhibition. In this study, we tested the effect of specific activation of neurons within the DMH and PeF on the baroreflex control of renal sympathetic nerve activity and heart rate in urethane-anesthetized rats. Microinjection of bicuculline (a GABA(A) receptor antagonist) into the DMH caused dose-dependent increases in heart rate and renal sympathetic activity, shifted the baroreflex control of both variables to higher levels (i.e., increased the upper and lower plateaus of the baroreflex function curves, and increased the threshold, midpoint, and saturation levels of mean arterial pressure). The maximum gain of the sympathetic component of the baroreflex was also increased, while that of the cardiac component was not significantly changed. Increases in the midpoint were very similar in magnitude to the evoked increases in baseline mean arterial pressure. Microinjection of bicuculline into the PeF evoked very similar effects. The results indicate that disinhibition of neurons in the DMH/PeF region not only increases sympathetic vasomotor activity and heart rate but also resets the baroreceptor reflex such that it remains effective, without any decrease in sensitivity, over a higher operating range of arterial pressure.     

Intermedin in the Paraventricular Nucleus Attenuates Cardiac Sympathetic Afferent Reflex in Chronic Heart Failure Rats

Background and Aim

Intermedin (IMD) is a member of calcitonin/calcitonin gene-related peptide (CGRP) family together with adrenomedullin (AM) and amylin. It has a wide distribution in the central nervous system (CNS) especially in hypothalamic paraventricular nucleus (PVN). Cardiac sympathetic afferent reflex (CSAR) is enhanced in chronic heart failure (CHF) rats. The aim of this study is to determine the effect of IMD in the PVN on CSAR and its related mechanisms in CHF rats.

Methodology/Principal Findings

Rats were subjected to left descending coronary artery ligation to induce CHF or sham-operation (Sham). Renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP) and heart rate (HR) were recorded. CSAR was evaluated by the RSNA and MAP responses to epicardial application of capsaicin. Acute experiments were carried out 8 weeks after coronary ligation or sham surgery under anesthesia. IMD and angiotensin II (Ang II) levels in the PVN were up-regulated in CHF rats. Bilateral PVN microinjection of IMD caused greater decreases in CSAR and the baseline RSNA and MAP in CHF rats than those in Sham rats. The decrease of CSAR caused by IMD was prevented by pretreatment with AM receptor antagonist AM22-52, but not CGRP receptor antagonist CGRP8-37. Ang II in the PVN significantly enhanced CSAR and superoxide anions level, which was inhibited by PVN pretreatment with IMD or tempol (a superoxide anions scavenger) in Sham and CHF rats.

Conclusion

IMD in the PVN inhibits CSAR via AM receptor, and attenuates the effects of Ang II on CSAR and superoxide anions level in CHF rats. PVN superoxide anions involve in the effect of IMD on attenuating Ang II-induced CSAR response.     

Rearrangement of scratch generator efferent activity during electrical activation of descending systems

Effects of signals proceeding along descending pathways on parameters of scratch generator activity were investigated in decerebrate immobilized cats. Certain phase-linked alterations in these parameters were shown to occur under the effects of electrical activation of the main descending systems. The biggest increase in scratch cycle duration under electrical stimulation of Deiter's nucleus, the red nucleus, and pyramidal tract is produced when stimuli are applied during the first half of the aiming stage. Stimulation during the second half of the aiming phase and at the start of the scratching movement hardly affect the scratching cycle. The main increase in length of scratch cycle during electrical stimulation of the reticular gigantocellularis nucleus is noted when stimuli are presented during the second half of the aiming stage. Electrical activation of descending pathways during the latter induces a rise in intensity in this phase and reduced intensity of the actual scratching stage. Activation of the pathways during this scratching motion causes heightened intensity of the motion while hardly affecting intensity of the aiming phase. The principles of suprasegmental rectification of scratch generator operation are discussed.A. A. Bogomolets Institute of Physiology, Academy of Sciences of the Ukrainian SSR, Kiev. Translated from Neirofiziologiya, Vol. 22, No. 3, pp. 300–309, May–June, 1990.     

Modulation of reflexsympathetic discharge by the cholinergic agonist oxotremorine and by clonidine

The cholinergic agonist oxotremorene can produce marked centrally-mediated cardiovascular effects. In past experiments in anesthetized cats, oxotremorine reduced blood pressure and an evoked sympathetic reflex. However, unlike other sympathetic inhibitors, it decreased sympathetic outflow selectively, did not slow heart rate but prolonged the latency of an evoked sympathetic reflex. In view of these striking differences, effects of oxotremorine on another reflex involved in cardiovascular control were assessed in anesthetized cats and compared to those produced by clonidine. Stimulation of the carotid sinus nerve with short duration pulses evoked reflex firing in the splanchnic nerve. Oxotremorine (50 – 800 ug/kg i.v.) caused a dose-related decrease in blood pressure and inhibited the evoked potential at the higher doses (200–800 ug/kg) but did not prolong its latency. Clonidine produced similar effects. Thus, attenuation by oxotremorine of an additional fundamental cardiovascular reflex was demonstrated. Seletcive inhibition of sympathetic outflow by oxotremorine as well as its differential effect on the latencies of cardiovascular reflexes indicates that the compound influences medullary and descending sympathetic pathways in a complex manner and suggests that the inhibition occurs at more than one site.     

Invariable H-reflex and sustained facilitation of stretch reflex with heightened sympathetic outflow

Stretch reflex shows sustained (3-min) increase with heightened sympathetic outflow [Hjortskov N, Skotte J, Hye-Knudsen C, Fallentin N. Sympathetic outflow enhances the stretch reflex response in the relaxed soleus muscle in humans. J Appl Physiol 2005;98:1366–70], but it is unknown if it accompanies a sustained increase in H-reflex. The purpose of the study was to test if there is a sustained facilitation in the H-reflex in the human soleus muscle during a variety of sustained tasks that are known to elevate sympathetic outflow. Mean arterial blood pressure, heart rate, and H- and stretch reflexes in the relaxed soleus muscle were obtained in healthy young adults who performed mental arithmetic, static handgrip exercise, post-handgrip ischemia, and cold stimulation. Each task lasted 3 min with a 3-min rest in between tasks. Data were analyzed for the initial 30 s and entire 3 min of each task. There was a heightened cardiovascular response in all tasks for both durations of analysis. An increase in H-reflex amplitude was not observed for either the initial or entire duration of the analysis. The tasks increased stretch reflex amplitude for both durations of analysis. Invariable H-reflex and sustained facilitation of stretch reflex with heightened sympathetic outflow would imply sympathetic modulation of muscle spindle sensitivity.     

Long systems of the dorsolateral fascicle: influence of afferentation from the splanchnic region.

The influence of afferentation from the splanchnic region on the activity of long systems in the dorsolateral fascicle (DLF) was studied in chloralose-anaesthetized cats. Ascending axons (the dorsal spinocerebellar tract, DSCT and the spinocervical tract, SCT) did not respond to splanchnic stimuli. Conditioning from the splanchnic region modified their activity; the effect (mainly inhibitory) was strongest in the case of exteroceptive channels. The reaction of long propriospinal neurones depended on whether they belonged to ascending or descending pathways. No responses to splanchic stimuli were observed in the axons of ascending (proprioceptive, exteroceptive) units and conditioning from the splanchnic region only modified their activity. In decending axons, synaptic discharges with a long latent period (over 20 msec) were generated. The interaction of inputs from the visceral and somatosensory regions resulted in reciprocal inhibition of the tested activity. In axons descending from suprasegmental areas, splanchnic afferentation generated synaptic discharges with a time course comparable to spino-bulbo-spinal activity. Interaction with the responses from somatic nerves resulted inhibition of the tested activity. The results confirmed that the splanchnic region participates in modifying and evoking activity in the long DLF systems.     

Ascending pathways mediating somatoautonomic reflexes in exercising dogs

The ascending spinal pathways mediating somatocardiovascular reflexes during exercise were studied in unanesthetized dogs by placing lesions in the lumbar spinal cord. After training to run on a treadmill with hindlimbs only, 20 dogs were anesthetized and instrumented using sterile surgical techniques. To chronically record heart rate and arterial blood pressure, the aorta was cannulated via the omocervical artery. To test the intactness of descending spinal sympathetic pathways, reflex pressor responses to baroreceptor hypotension were produced by bilateral carotid arterial occlusion using pneumatic vessel occluders placed around the common carotid arteries. To generate transient ischemic exercise (120 s), a pneumatic occluder was placed around the left iliac artery. Eight to 10 days after instrumentation, blood pressure and heart rate were monitored at rest and during hindlimb running with and without simultaneous iliac arterial occlusion. The modest pressor response and tachycardia elicited by hindlimb exercise were markedly augmented by simultaneous hindlimb ischemia (i.e., iliac arterial occlusion). Lesion placement in the dorsolateral sulcus area and the dorsolateral funiculus at L2 significantly reduced the blood pressure and heart rate responses to simultaneous exercise occlusion. The cardiovascular responses to nonischemic exercise and bilateral carotid arterial occlusion were not altered by such spinal sections. It is concluded that in the dog the ascending spinal pathways mediating cardiovascular responses to ischemic exercise are located in the lateral funiculus, including the dorsolateral sulcus area and dorsolateral funiculus.     

Cardiac Rhythm Variability: Approaches to Mechanisms

Physiological mechanisms of cardiac rhythm variability (CRV) are reviewed. The results of original experiments are discussed together with the history of the problem and data available from the literature. Special emphasis is placed on the spectral analysis of cardiac rhythm. Various mechanisms of the generation of periodic and aperiodic components of CRV are considered. Although the variability of cardiac rhythm has been studied for many years in many laboratories worldwide, fine mechanisms of CRV remain obscure. However, a number of specific features of CRV are presently widely recognized. Periodic CRV components isolated from short-term records in patients at rest are represented by high-frequency, low-frequency, and very low-frequency oscillations. Fourier-transform spectral analysis of cardiac rhythm is the most appropriate method of the detection of these oscillations. High-frequency components are associated with respiration and represent the effects of the parasympathetic nervous system on myocardium. Low-frequency components are due to the activity of the postganglionic sympathetic fibers and represent the processes of cardiac rhythm modulation by the sympathetic nervous system. Genesis of very low-frequency oscillations is still uncertain. Most probably, these oscillations are associated with the effects of suprasegmental (primarily, hypothalamic) centers of autonomic regulation. Aperiodic CRV components represent random events associated with the reflex regulation of the heart rate by external or internal factors. Because aperiodic components significantly modify the results of the CRV analysis, the effects of these factors should be eliminated. It is concluded that because many problems associated with cardiac rhythm variability remain to be solved, extensive research in this direction should be continued.     

Respiratory modulation of the startle reflex in cats

Phase respiratory influences on reflex after-discharges in response to stimulation of the segmental nerves as well as tactile and acoustic stimulation in the limb and intercostal nerves — physiological analogs of startle reflexes (SR) were studied in unanesthetized (decerebrate) or chloralose-anesthetized cats. It was found that the level of these reflexes in the inhalation phase of respiration was 8–58% lower than during exhalation. The difference between the inhalation and exhalation phases was determined for different types of reflexes and under varying experimental conditions. Evidence was obtained that respiratory modulation of reflexes occurs mainly at the level of suprasegmental (reticular) mechanisms. Clear distinctions could be drawn between the pattern of reflex modulation in the lower intercostal nerves and those of the limbs. Findings would lead to the conclusion that the likely mechanisms underlying suprasegmental respiratory influences on these reflexes differ, as does the organization of their reticular centers.S. V. Kurashov Medical Institute, Ministry of Public Health of the RSFSR, Kazan'. Translated from Neirofiziologiya, Vol. 18, No. 5, pp. 593–603, September–October, 1986.     

Comparative study of sympathetic and parasympathetic firing in automatic nerves produced by stimulating different structures of the cat hypothalamus

It was discovered by making simultaneous recordings of evoked hypothalamic-parasympathetic and hypothalamic-sympathetic firing that sympathetic discharges in the splanchnic nerve and parasympathetic discharges in the pelvic nerve with minimum latency and lowest threshold level could be obtained by stimulating the posterolateral hypothalamus. It was also found that the focus of maximum neuronal activity produced by stimulating afferent visceral nerve fibers as well as the highest concentration of evoked efferent response in sympathetic and parasympathetic nerves were located in the same hypothalamic area. A working hypothesis was put forward that convergent polysensory hypothalamic neurons also act as divergent polyeffector constituents of the integrative system of the hypothalamovisceral reflex arc.L. A. Orbeli Institute of Physiology, Academy of Sciences of the Armenian SSR, Erevan. Translated from Neirofiziologiya, Vol. 19, No. 4, pp. 482–491, July–August, 1987.     

Insights into mechanisms of intestinal segmentation in guinea pigs: a combined computational modeling and in vitro study

Segmentation in the guinea pig small intestine consists of a number of discrete motor patterns including rhythmic stationary contractions that occur episodically at specific locations along the intestine. The enteric nervous system regulates segmentation, but the exact circuit is unknown. Using simple computer models, we investigated possible circuits. Our computational model simulated the mean neuron firing rate in the feedforward ascending and descending reflex pathways. A stimulus-evoked pacemaker was located in the afferent pathway or in a feedforward pathway. Output of the feedforward pathways was fed into a simple model to determine the response of the muscle. Predictions were verified in vitro by using guinea pig jejunum, in which segmentation was induced with luminal fatty acid. In the computational model, local stimuli produced an oral contraction and anal dilation, similar to in vitro responses to local distension, but did not produce segmentation. When the stimulus was distributed, representing a nutrient load, the result was either a tonic response or globally synchronized oscillations. However, when we introduced local variations in synaptic coupling, stationary contractions occurred around these locations. This predicts that severing the ascending and descending pathways will induce stationary contractions. An acute lesion in our in vitro model significantly increased the number of stationary contractions immediately oral and anal to the lesion. Our results suggest that spatially localized rhythmic contractions arise from a local imbalance between ascending excitatory and descending inhibitory muscle inputs and require a distributed stimulus and a rhythm generator in the afferent pathway.     

The role of reflex mechanisms in postinhibitory rebound studied by analysis of human single motor unit activity

The mechanism of onset of rebound after inhibition induced by electrical stimulation of a nerve of maximal and submaximal strength for M-response was studied in single motor units of normal human soleus, rectus femoris, and hand muscles. Poststimulus histograms and changes in the duration of interspike intervals were compared with mechanical recordings of muscle contractions. In all muscles tested, during strong isotonic contraction, the increase in motor unit activity after a silent period was partly due to synchronization of their emergence from inhibition. However, it also contained a component of true facilitation of motoneurons, which was evidently a reflex response to lengthening of the muscle in the relaxation phase after evoked contraction. The latent period of this facilitation in the soleus and rectus femoris muscles coincided in value with the latent period of the monosynaptic spinal reflex, whereas in the hand muscles, in which a monosynaptic response to electrical nerve stimulation could not be evoked, the latent period of facilitation as a result of spindle activation during muscle relaxation was significantly longer than the latent period of the monosynaptic reflex. These findings support the hypothesis of presynaptic suppression of monosynaptic connections of Ia afferents with the motoneurons of some human muscles by descending tonic influences and of the use of information coming from spindles by supraspinal levels of the CNS.     

Functional characteristics of the intraspinal spread of viscerosomatic activity.

The functional characteristics of the intraspinal spread of the dual-component viscerosomatic reflex response were studied in chloralose-anaesthetized cats. In the region of the direct inputs of splanchnic afferents into the spinal cord, the initial part of the early (propriospinal) component is evoked by afflux from the extraspinal pathway in the sympathetic chain and has the shortest latent period. At segment Th8 to Th12 level this was 5.2--8.1 msec; cranially and caudally from this level it was longer. Activity spreading from the adjacent segments via intraspinal longitudinal systems also participates in the origin and course of the early component of the efferent discharge. The rate of ascending intraspinal irradiation in the thoracic region was 3.2--12 m/sec (6.6 +/- 2.4 m/sec). The rate of the descending spread of propriospinal activity in the thoracic region via intraspinal pathways was 3.6--18.3 m/sec (12.5 +/- 4.5 m/sec); in the lumbar region it was significantly lower -- 2.9--19.3 m/sec (7 +/- 4.5 m/sec). The latent period of the later component varied from 20 to 30 msec and displayed a cranio-caudal increase in length. The rate of the descending spread of the later component in the thoracic and lumbar cord did not differ significantly (20 +/- 10 m/sec and 22 +/- 13 m/sec respectively). The continuous splanchnic discharge in the lumbosacral region is correlated to the different rate of the intraspinal spread of the early and the late response and to their overlapping.