[Improvement of indications for nephropexy through combined isotope examination of kidneys and afferent urinary pathways].
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Redistribution of blood volume during orthostatism is followed by a reduction in venous return and therefore cardiac output. A drop in the blood pressure following postural changes is normally prevented by the action of the baroreceptor reflex, which leads to an increase in total peripheral resistance and heart rate. Orthostatic hypotension may arise from a variety of causes. In some cases, the disorder of postural regulation is due to an autonomic nervous system disease, and various tests are available that enable the diagnosis to be confirmed and the mechanism of action to be elucidated. Certain of these investigations explore the function of the complete baroreceptor reflex arc, while others enable selective study of either the efferent parasympathetic or sympathetic pathways. Central zones and afferent pathways cannot be explored directly. Individual tests are of limited value only, and the results of overall investigations are necessary for a better understanding and therefore more effective therapy of orthostatic hypotension due to autonomic nervous system disease.
The effects of tendon vibration on bioassayable growth hormone (BGH) secretion from the pituitary gland were investigated in anesthetized adult male rats. The tendons from predominantly fast-twitch ankle extensor muscles (gastrocnemius and plantaris) or a predominantly slow-twitch ankle extensor (soleus) were vibrated by using a paradigm that selectively activates group Ia afferent fibers from muscle spindles. The lower hindlimb was secured with the muscles near physiological length, and the tendons were vibrated for 15 min at 150 Hz and a displacement of 1 mm. Control rats were prepared similarly, but the tendons were not vibrated. Compared with control, vibration of the tendons of the fast ankle extensors markedly increased (160%), whereas vibration of the slow soleus decreased (68%), BGH secretion. Complete denervation of the hindlimb had no independent effects on the normal resting levels of BGH, but it prevented the effects of tendon vibration on BGH secretion. The results are consistent with previous findings showing modulation of BGH release in response to in vivo activation or in situ electrical stimulation of muscle afferents (Bigbee AJ, Gosselink KL, Grindeland RE, Roy RR, Zhong H, and Edgerton VR. J Appl Physiol 89: 2174-2178, 2000; Gosselink KL, Grindeland RE, Roy RR, Zhong H, Bigbee AJ, and Edgerton VR. J Appl Physiol 88: 142-148, 2000; Gosselink KL, Grindeland RE, Roy RR, Zhong H, Bigbee AJ, Grossman EJ, and Edgerton VR. J Appl Physiol 84: 1425-1430, 1998). These data provide evidence that this previously described muscle afferent-pituitary axis is neurally mediated via group Ia afferents from peripheral skeletal muscle. Furthermore, these data show that activation of this group Ia afferent pathway from fast muscles enhances, whereas the same sensory afferent input from a slow muscle depresses, BGH release.
1. Sulphated glycoprotein output from the trachea, isolated in situ, has been measured in anaesthetized cats by a radio-isotopic method. The effects of irritation of various parts of the airway on this mucus output were studied. 2. Mechanical stimulation of the nose and nasopharynx increased tracheal mucus output by reflexes which involved parasympathetic and probably also sympathetic motor pathways. 3. Laryngeal stimulation had a similar through the same motor pathways. 4. Inhalation of ammonia vapour into the lower airways reflexly increased mucus output from the isolated trachea. The efferent pathway for this reflex was mainly or entirely parasympathetic. It is argued that the afferent pathway involved cough receptors. 5. Lung inflation, inhalation of histamine aerosol and intravenous injection of phenyl diguanide (which excite mainly lung stretch receptors, lung 'irritant' receptors and alveolar 'J-receptors' respectively) had no consistent effect on tracheal mucus secretion. 6. The afferent and efferent pathways of these reflexes are discussed.
1. Intracellular recording from motoneurones to hind limb muscles in the cat was used to investigate the effect of volleys in the posterior nerve to the knee joint on motoneurones and on transmission from Ib afferents. 2. Volleys in the joint nerve facilitate transmission in disynaptic and trisynaptic inhibitory and excitatory reflex pathways from Ib afferents. It is postulated that facilitation, which appears at a strength of 1.5 times threshold, is evoked, not by Ib afferents which 'contaminate' the joint nerve, but by afferents from joints receptors. 3. T;e time course of facilitation of the disynaptic Ib i.p.s.p.s in motoneurones indicates that these joint afferents have disynaptic connexions with the interneurones of the Ib inhibitory pathway. 4. A brief description is given of synaptic effects evoked in motoneurones by graded electrical stimulation of the posterior nerve to the knee joint. At low stimulus strength the effects may be evoked via interneurones of Ib reflex pathways, but some results suggest that other interneuronal paths are utilized as well. Somewhat higher strengths, but occasionally less than 2 times threshold, produce later synaptic effects presumably mediated by reflex paths from the flexor reflex afferents; it does not seem likely that the contributory afferents in the joint nerve have nociceptive function. 5. It is suggested that impulses from impulses from joint receptors can influence tension regulation from Golgi tendon organs; if these receptors are activated in the terminal phase of the movement they may contribute a purposeful decrease of tension. It is pointed out that joint receptors may have an important role in motor regulation by their effects on interneurones of the different neuronal systems controlling motoneurones.
We examined the effect of iontophoretic application of bicuculline methiodide and strychnine hydrochloride on the mesencephalic locomotor region (MLR)-induced inhibition of dorsal horn cells in paralyzed cats. The activity of 60 dorsal horn cells was recorded extracellularly in laminae I, II, V-VII of spinal segments L7-S1. Each of the cells was shown to receive group III muscle afferent input as demonstrated by their responses to electrical stimulation of the tibial nerve (mean latency and threshold of activation: 20.1+/-6.4 ms and 15.2+/-1.4 times motor threshold, respectively). Electrical stimulation of the MLR suppressed transmission in group III muscle afferent pathways to dorsal horn cells. Specifically the average number of impulses generated by the dorsal horn neurons in response to a single pulse applied to the tibial nerve was decreased by 78+/-2.8% (n=60) during the MLR stimulation. Iontophoretic application (10-50 nA) of bicuculline and strychnine (5-10 mM) suppressed the MLR-induced inhibition of transmission of group III afferent input to laminae I and II cells by 69+/-5% (n=10) and 29+/-7% (n=7), respectively. Likewise, bicuculline and strychnine suppressed the MLR-induced inhibition of transmission of group III afferent input to lamina V cells by 59+/-13% (n=14) and 39+/-11% (n=10), respectively. Our findings raise the possibility that GABA and glycine release onto dorsal horn neurons in the spinal cord may play an important role in the suppression by central motor command of thin fiber muscle afferent-reflex pathways.
The organization of transient projections from the primary somatosensory cortex (S-I) to the cerebellar cortex in neonatal kittens was examined using orthograde intraaxonal labeling techniques. Tritiated amino acid injections into face, forelimb and hindlimb areas of representation in S-I labeled mossy fiber-like terminals of cerebrocerebellar axons in different areas of the cerebellar cortex bilaterally. The hindlimb area of S-I projected to lobules I-IV in the anterior lobe and to ventral folia of the paramedian lobule (PML). Injections into forelimb areas of S-I labeled terminals in lobules IV and V and in intermediate and dorsal folia of the PML. The face area of S-I projected to the lobules V and VI, to medial folia in the ansiform and simplex lobules and to dorsal PML folia. Labeled terminals were more numerous in the cerebellar cortex contralateral to the S-I injections, except in lobules I and II and the ventral PML where the density of hindlimb input was approximately the same on both sides. These observations were supplemented by findings that small wheat germ agglutinin-horseradish peroxidase (WGA-HRP) injections into the dorsal or ventral PML resulted in retrogradely labeled layer V pyramidal neurons in lateral (face and forelimb) and medial (hindlimb) areas of S-I respectively. The somatotopic organization of transient S-I cerebrocerebellar projections is very similar to the topography of cerebellar somatosensory afferent pathways in adult cats.
By the comparison of nerve action potentials and cerebral potentials evoked by the same electrical stimulus the propagation of the somaesthetic impulse to the cerebral cortex can be evaluated. This technique was applied to the fibres of the sural nerve in normal subjects and in patients presenting various lesions of the peripheral and central nervous system. Evoked cerebral potential afforded valuable data when it was not possible to record the nerve action potentials or when the lesion involved the central segment of the afferent pathway.
BACKGROUND: Hydrochloric acid (HCl) is a potential threat to the integrity of the gastric mucosa and is known to contribute to upper abdominal pain. We have previously found that gastric mucosal challenge with excess HCl is signalled to the rat brainstem, but not spinal cord, as visualized by expression of c-fos messenger ribonucleic acid (mRNA), a surrogate marker of neuronal excitation. This study examined whether gastric mucosal exposure to capsaicin, a stimulant of nociceptive afferents that does not damage the gastric mucosa, is signalled to both brainstem and spinal cord and whether differences in the afferent signalling of gastric HCl and capsaicin challenge are related to different effects on gastric emptying. RESULTS: Rats were treated intragastrically with vehicle, HCl or capsaicin, activation of neurons in the brainstem and spinal cord was visualized by in situ hybridization autoradiography for c-fos mRNA, and gastric emptying deduced from the retention of intragastrically administered fluid. Relative to vehicle, HCl (0.5 M) and capsaicin (3.2 mM) increased c-fos transcription in the nucleus tractus solitarii by factors of 7.0 and 2.1, respectively. Capsaicin also caused a 5.2-fold rise of c-fos mRNA expression in lamina I of the caudal thoracic spinal cord, although the number of c-fos mRNA-positive cells in this lamina was very small. Thus, on average only 0.13 and 0.68 c-fos mRNA-positive cells were counted in 0.01 mm sections of the unilateral lamina I following intragastric administration of vehicle and capsaicin, respectively. In contrast, intragastric HCl failed to induce c-fos mRNA in the spinal cord. Measurement of gastric fluid retention revealed that HCl suppressed gastric emptying while capsaicin did not. CONCLUSION: The findings of this study show that gastric mucosal exposure to HCl and capsaicin is differentially transmitted to the brainstem and spinal cord. Since only HCl blocks gastric emptying, it is hypothesized that the two stimuli are transduced by different afferent pathways. We infer that HCl is exclusively signalled by gastric vagal afferents whereas capsaicin is processed both by gastric vagal and intestinal spinal afferents.
Muscle afferent activity from the triceps surae was recorded during experimentally induced alterations in amplitude of the Achilles tendon jerk. No changes in the neural afferent response to tendon percussion or in the background level of neural activity occurred when the reflex response was altered by discomfort, distraction, changes in attention, or changes in the rate of tendon percussion. Reinforcement of the Achilles tendon jerk by forceful contraction of the forearm muscles did not alter the relationship between intensity of the tendon tap and amplitude of the evoked neural afferent volley. Nevertheless, such maneuvers lowered the reflex threshold and raised reflex sensitivity so that a smaller afferent volley was required to produce a tendon jerk, and an increase in the afferent volley produced a disproportionately greater increase in reflex electromyographic activity than would have occurred at rest. Reinforcement maneuvers potentiated the H-reflex but did not alter the electrically induced afferent volley or the background level of neural activity. It is concluded that these changes in reflex responsiveness occurred through intrinsic spinal mechanisms independent of the fusimotor system.
Selective lesions of discrete aminergic and cholinergic afferent pathways to the hippocampal formation have been studied as an experimental model of behavioral recovery after partial hippocampal deafferentation in adult rats. The noradrenergic, serotoninergic and cholinergic afferents reach the hippocampal formation along three routes: a supracallosal pathway, a subcallosal pathway (along the fimbria-fornix), and a ventral pathway (along the ansa lenticularis and the ventral amygdaloid pathway). Bi-lateral lesion of the supracallosal pathway resulted in significant reductions in biochemical markers of the hippocampal noradrenergic, serotoninergic and cholinergic innervations. Within 6 weeks following lesion these markers were found to have recovered to levels close to normal. A more substantial deafferentation, obtained by a bilateral lesion of both dorsal pathways, resulted in a more profound initial decrease in the biochemical marker levels, and a less complete recovery in the long-term animals. Concomitant with the initial phase of deafferentation, rats with lesions of one or both of the dorsal afferent pathways exhibited an equally profound behavioral deficit in acquisition of a forced choice alternation learning task in a T-maze. However, while rats subjected to the combined supracallosal-fimbria-fornix lesion remained impaired, the ones with lesions of the supracallosal pathway alone exhibited a significant recovery of the capacity to perform the maze task. The correlation between behavioral recovery and recovery of the biochemical markers in the supracallosal pathway-lesioned group was significant for the serotoninergic innervation of the hippocampus. The present results suggest that reinnervation of the partially deafferented hippocampus through compensatory collateral sprouting is a valuable new experimental model system within which to analyze mechanisms underlying functional recovery after lesions in the CNS.
Intravenous infusion of blood (36 ml/kg body wt) elicited tachycardia in artificially ventilated anesthetized dogs with intact autonomic innervation and in dogs with cardiac beta-receptor blockade. In contrast, infusion elicited bradycardia in dogs with section of the spinal cord at C6-C7, and in dogs with combined spinal section and cardiac beta-receptor blockade. The control heart rate was less than or equal to 110 beats/min in all the animals. The presence of infusion-induced tachycardia in dogs with beta-receptor blockade, i.e., dogs in which cardiac sympathetic efferents were blocked, and its absence in dogs with combined spinal section and beta-receptor blockade, i.e., dogs in which spinal autonomic afferents plus cardiac sympathetic efferents were blocked, may be the result of an additional interruption of spinal autonomic afferents by spinal section. It is concluded that tachycardia elicited by infusion may be partly due to a reflex with its afferent pathway in the spinal cord and its efferent pathway in the vagus nerves.
Glutamate is a major neurotransmitter of chemoreceptor and baroreceptor afferent pathways in mammals and therefore plays a central role in the development of cardiorespiratory reflexes. In fish, the gills are the major sites of these receptors, and, consequently, the terminal field (sensory area) of their afferents (glossopharyngus and vagus) in the medulla must be an important site for the integration of chemoreceptor and baroreceptor signals. This investigation explored whether fish have glutamatergic mechanisms in the vagal sensory area (Xs) that could be involved in the generation of cardiorespiratory reflexes. The locations of the vagal sensory and motor (Xm) areas in the medulla were established by the orthograde and retrograde axonal transport of the neural tract tracer Fast Blue following its injection into the ganglion nodosum. Glutamate was then microinjected into identified sites within the Xs in an attempt to mimic chemoreceptor- and baroreceptor-induced reflexes commonly observed in fish. By necessity, the brain injections were performed on anaesthetised animals that were fixed by 'eye bars' in a recirculating water system. Blood pressure and heart rate were measured using an arterial cannula positioned in the afferent branchial artery of the 3rd gill arch, and ventilation was measured by impedance probes sutured onto the operculum. Unilateral injection of glutamate (40-100 nl, 10 mmol l(-1)) into the Xs caused marked cardiorespiratory changes. Injection (0.1-0.3 mm deep) in different rostrocaudal, medial-lateral positions induced a bradycardia, either increased or decreased blood pressure, ventilation frequency and amplitude and, sometimes, an initial apnea. Often these responses occurred simultaneously in various different combinations but, occasionally, they appeared singly, suggesting specific projections into the Xs for each cardiorespiratory variable and local determination of the modality of the response. Response patterns related to chemoreceptor reflex activation were predominantly located rostral of obex, whereas patterns related to baroreceptor reflex activation were more caudal, around obex. The glutamate-induced bradycardia was N-methyl-D-aspartate (NMDA) receptor dependent and atropine sensitive. Taken together, our data provide evidence that glutamate is a putative player in the central integration of chemoreceptor and baroreceptor information in fish.
Neurophysiological assessment of breathing is mandatory for the diagnosis and management of respiratory problems occurring in neuromuscular disorders (neuromuscular complications of critical illness, spinal cord trauma, C4-C5 radiculopathies, phrenic nerve neuropathy, diabetes mellitus, Guillain-Barré syndrome etc...). We review the methods of exploration (principles and normative data) of efferent pathways (phrenic nerve conduction, central motor conduction studies with transcranial magnetic stimulation, diaphragmatic EMG) and afferent pathways (somatosensory evoked potentials of the phrenic nerve, respiratory evoked potentials, sympathetic skin response during sudden occlusion of respiratory pathways during inspiration), as well as their main indications.
In 48 patients who had neurosensory hypoacusia and whose main complaint was tinnitus, a 1% pilocarpine solution or a 2% carbachol Isopto solution was placed in the tympanic cavity by means of a No. 26 pencil-tipped lumbar puncture needle through the front quadrant of the eardrum. Patients were chosen without regard for age, gender, or topographical damage of the acoustic pathway. Evaluation of the drug's effect was performed audiometrically by masking with the minimum intensity of the pure sound or narrow band that most closely resembled the patients' own noises. The results of this medical therapy were positive and ranged from complete annulment to attenuation of the tinnitus, which was confirmed by audiometric masking 30 minutes after the intratympanic injection. These positive results reached 50% and would have been higher if the several cases submitted by accident insurance companies and cases of presbyacusia were discarded. The unsatisfactory element of the study was the short-term effect of the therapy, which usually lasted no more than 12-72 hours. Tinnitus reappeared in all patients at its original intensity. The best results involved the use of carbachol as compared with pilocarpine. The decision to replace pilocarpine with carbachol was based on the idea that the inhibitory cholinergic efferent pathways are damaged before the afferent pathways. The use of pilocarpine depends on efficient cholinergic functioning, as its activity is as an indirect agonist (i.e., to annul the cholinesterase enzyme).
This study tests three hypotheses regarding mechanisms that produce rapid shallow breathing during a severe inspiratory resistive load (IRL): 1) an intact vagal afferent pathway is necessary; 2) diaphragm fatigue contributes to tachypnea; and 3) hypoxia may alter the pattern of respiration. We imposed a severe IRL on pentobarbital sodium-anesthetized dogs, followed by bilateral vagotomy, then by supplemental O2. IRL alone produced rapid shallow breathing associated with hypercapnia and hypoxia. After the vagotomy, the breathing pattern became slow and deep, restoring arterial PCO2 but not arterial PO2 toward the control values. Relief of hypoxia had no effect, and at no time was there any evidence of fatigue of the diaphragm as measured by the response to phrenic nerve stimulation. We conclude that an intact afferent vagal pathway is necessary for the tachypnea resulting from a severe IRL, neither hypoxia nor diaphragm fatigue played a role, and, although we cannot rule out stimulation of vagal afferents, the simplest explanation for the increased frequency in our experiments is increased respiratory drive due to hypercapnia.
The neural integration of afferent inputs evoked by spatiotemporally distributed sensory stimuli is a critical step in the formation of coherent and continuous perceptual representations. Integration mechanisms in various systems include linear and nonlinear summation of sensory responses. One well-known example in the rat barrel system is the suppressive interaction between responses to the consecutive deflection of neighboring whiskers. The mechanism underlying cross-whisker suppression has long been postulated to rely on intracortical postsynaptic inhibition, although this hypothesis has been challenged by recent reports. Here we show, using intracellular and extracellular recordings in vivo, that cross-whisker suppression occurs in the absence of cortical activity. Instead, suppression arises from local circuit operations at multiple levels of the subcortical afferent pathway and is amplified by the nonlinear transformation of synaptic input into spike output in both the thalamus and cortex. Because these cellular processes are common to neural circuits subserving visual and auditory modalities, we propose that the suppressive mechanisms elucidated here are a general property of thalamocortical sensory systems.