Thalamic pathway for rapid afferent input from hand to motor cortex in the monkey [proceedings].
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Afferent Pathways↗
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A confocal and electron microscopic study of contacts between 5-HT fibres and feline dorsal horn interneurons in pathways from muscle afferents.
Morphological substrates of actions of serotonin upon dorsal horn interneurons with input from group II muscle afferents were investigated by using two experimental approaches. Twelve interneurons were intracellularly labelled with rhodamine-dextran, and serotoninergic fibres were identified by immunofluorescence. Appositions between the serotoninergic axons and these interneurons were examined with a dual-channel confocal microscope. A further four interneurons were intracellularly labelled with horseradish peroxidase, and serotoninergic axons were identified by immunocytochemistry; these neurons were prepared for combined light and electron microscopy. Confocal microscopy revealed serotoninergic varicosities in apposition to both cell bodies and dendrites. Similar total numbers of appositions were found on the soma, and on dendrites within 100 microm from the soma, on the most completely labelled neurons. The number of appositions on 100-microm segments of dendrites decreased with increasing distances from the soma (from 14.6 within 100 microm, to 3.8 and 2.4 at 100-300 microm, and more than 300 microm distances, respectively). Electron microscopic analysis of two neurons revealed that few of the apparent contacts on cell bodies were synaptic, but, in contrast, many varicosities apposed to proximal dendrites formed synapses. The evidence suggests that serotonin may have more powerful synaptic effects upon the dendrites of this class of dorsal horn interneurons than on their cell bodies.
Afferent Pathways↗
Electrophysiological investigations on the mode of action of nefopam, a novel analgesic agent.
The mode of action of nefopam, a novel analgesic, on the splanchnic afferent pathway was investigated using electrophysiological methods. Nefopam (2.5 and 5.0 mg/kg, i.v.) caused arousal patterns in spontaneous rabbit EEG. In intact cats, nefopam (1.0, 2.5 and 5.0 mg/kg, i.v.) suppressed the evoked potentials recorded from the posterior sigmoid gyrus of the cortex, N. ventralis posterolateralis and N. centralis medialis of the thalamus and the ventrolateral funiculus of the spinal cord following splanchnic nerve stimulation without inhibiting potentials in the thalamocortical pathways. These depressant effects were not antagonized by a narcotic antagonist, levallorphan (0.5 mg/kg, i.v.). The inhibitory effect of nefopam on the spinal potential evoked by splanchnic nerve stimulation was not observed in spinal cats (C1-C2 transection) and pentobarbital-anesthetized cats. These results suggest that nefopam may inhibit the splanchnic afferent pathways in the spinal cord by reinforcing descending inhibitory systems originating in the supra-spinal structure, in a manner which differs from that seen with morphine.
Afferent Pathways↗
Pancreatic secretion evoked by cholecystokinin and non-cholecystokinin-dependent duodenal stimuli via vagal afferent fibres in the rat.
1. We have recently demonstrated that cholecystokinin (CCK) at physiological levels stimulates pancreatic enzyme secretion via gastroduodenal mucosal vagal afferent fibres in the rat. The present study was designed to investigate if non-CCK-mediated pancreatic stimuli which activate duodenal receptors also utilize similar vagal afferent pathways. 2. Intraduodenal administration of maltose (300 mM), hypertonic saline (500 mosmol l-1) and mucosal light stroking in anaesthetized rats evoked 70, 57 and 200% increases, respectively, in pancreatic protein secretion with no changes in plasma CCK concentration. Administration of the CCK receptor antagonist L364,718 did not affect pancreatic secretion evoked by these luminal stimuli. 3. Administration of atropine, acute vagotomy and duodenal mucosal application of capsaicin each completely abolished the pancreatic response to these stimuli. 4. Infusion of a subthreshold dose of the octapeptide of CCK (15 pmol (kg body wt)-1 h-1) potentiated the pancreatic response to duodenal infusion of maltose (300 mM) and hypertonic saline (500 mosmol l-1). 5. In conscious rats, perivagal application of capsaicin abolished the pancreatic response evoked by physiological doses of CCK and intraduodenal administration of maltose or hypertonic saline, confirming the physiological relevance of the observations in anaesthetized rats. 6. These results suggest that like CCK, non-CCK-mediated luminal stimuli evoke pancreatic enzyme secretion via stimulation of a vagal afferent pathway originating from the duodenal mucosa.
Afferent Pathways↗
Autonomic afferents at T1 in elicitation of volume-induced tachycardia in the dog.
Intravenous infusion of blood elicited tachycardia in anesthetized dogs with beta-receptor blockade (dogs with vagal efferents intact but cardiac sympathetic efferents blocked) and bradycardia in dogs with combined beta-receptor blockade and rhizotomy at T1 (dogs with vagal efferents intact but cardiac sympathetic efferents plus autonomic afferents at T1 blocked). This suggests that tachycardia elicited by volume in infusion may be partly due to a reflex with its afferent pathway at the T1 segment of the spinal cord and its efferent pathway in the vagi. Moreover, infusion evoked bradycardia in dogs with right-sided rhizotomy at T1, which was not significantly different from the response elicited in dogs with bilateral rhizotomy at T1. Additionally, the tachycardia response induced in dogs with ventral or dorsal rhizotomy at T1 was significantly different from the bradycardia response elicited in dogs with both dorsal and ventral rhizotomy at T1. These results suggest that the afferent pathway predominates on the right side, and its entry at T1 may be via both dorsal and ventral roots.
Afferent Pathways↗
Vagal afferent input from the acid-challenged rat stomach to the brainstem: enhancement by interleukin-1beta.
Exposure of the gastric mucosa to back-diffusing concentrations of HCl (0.25 M, pH 0.51) stimulates vagal afferent input to the brainstem. Here we have examined whether pretreatment of rats with the proinflammatory cytokines interleukin-1beta and tumor necrosis factor-alpha causes sensitization of vagal afferent pathways to HCl. Rats were pretreated i.p. with interleukin-1beta, tumor necrosis factor-alpha (10 microg/kg) or their vehicle (sterile saline) 24, 48 and 96 h before intragastric administration of HCl (0.25 M, 1 ml/100 g). Activation of neurons in the nucleus tractus solitarii was visualized by c-Fos immunohistochemistry 2 h after the HCl challenge. I.p. administration of interleukin-1beta and tumor necrosis factor-alpha alone induced c-Fos in the brainstem, an effect that was gone after 24 h. At this time, however, the effect of HCl to cause expression of c-Fos in the nucleus tractus solitarii was significantly enhanced by pretreatment with interleukin-1beta and tumor necrosis factor-alpha. The sensitizing effect of i.p.-administered interleukin-1beta was sustained for more than 48 h and prevented by the interleukin-1 receptor antagonist anakinra. Intracisternal administration of interleukin-1beta and tumor necrosis factor-alpha (100 ng) failed to amplify the HCl-evoked expression of c-Fos in the brainstem. These results show that peripheral administration of the proinflammatory cytokines interleukin-1beta and tumor necrosis factor-alpha induces prolonged sensitization of vagal afferent pathways to gastric HCl challenge. This effect seems to arise from a peripheral action on vagal afferents and may be of relevance to gastric chemonociception.
Afferent Pathways↗
Capsaicin-sensitive vagal afferents and CCK in inhibition of gastric motor function induced by intestinal nutrients.
The role of vagal afferent pathways and cholecystokinin (CCK) in mediating changes in gastric motor function after a meal was investigated in urethane-anesthetized rats. Proximal gastric motor function was measured manometrically, and nutrients were infused into an isolated segment of duodenum. Inhibition of gastric motility in response to duodenal infusion of protein (peptone or casein), but not carbohydrate (glucose), was significantly attenuated by administration of the CCK antagonist, L364,718. Selective ablation of vagal afferents by perineural treatment with the sensory neurotoxin, capsaicin, significantly reduced responses to both duodenal protein and glucose. These results suggest that protein in the duodenum decreases proximal gastric motor function via release of CCK and a vagal capsaicin-sensitive afferent pathway. In contrast, glucose acts via a capsaicin-sensitive vagal pathway not involving CCK. Thus separate neural and hormonal mechanisms mediate the effects of different nutrients in the duodenal feedback regulation of gastric motor function.
Afferent Pathways↗
Modulation of vagal efferent fibre discharge by mechanoreceptors in the stomach, duodenum and colon of the ferret.
1. A single-fibre-dissection technique was used to investigate the reflex modulation of vagal efferent fibre discharge by afferent fibres from various parts of the gastrointestinal tract of the urethane-anaesthetized ferret. 2. All but four of the 168 efferent fibres isolated in this study were spontaneously active. The majority of these had discharge frequencies of less than 6 spikes/sec. 3. All the efferent units received an afferent input from mechanoreceptors in the stomach. Two main types of response to gastric distension were seen: (i) an increase in efferent discharge and (ii) a decrease or complete suppression of efferent discharge. 4. The vagal efferent discharge was also modulated by duodenal and colonic distension, with the major effect being one of inhibition. 5. Bilateral vagotomy completely abolished the response to gastric distension in 68% of the units tested. The response to colonic and duodenal distension, however, was relatively unaffected by vagotomy. Thus the vagus provides the major afferent pathway from the stomach to these vagal efferent fibres, whilst the major input from the duodenum and colon is via a non-vagal pathway. Both vagal and splanchnic afferents therefore converge on to the vagal nucleus. 6. The destinations of these vagal efferent fibres and their possible functions are discussed.
Action Potentials↗
A functional neuroanatomy of anxiety and fear: implications for the pathophysiology and treatment of anxiety disorders.
This paper reviews the evidence that provides the basis for a functional neuroanatomy of anxiety and fear. The afferent arm of the anxiety circuit includes the exteroceptive sensory systems of the brain, which convey the sensory information contained in a fear- or anxiety-inducing stimulus to the dorsal thalamus. Visceral afferent pathways alter the function of the locus coeruleus and the amygdala. The thalamus relays sensory information to the primary sensory receptive areas of the cortex, which project to adjacent unimodal and polymodal cortical association areas. The cortical association areas send projections to the amygdala, entorhinal cortex, orbitofrontal cortex, and cingulate gyrus. A pivotal role for the amygdala in the transmission and interpretation of fear and anxiety is suggested by extensive afferents to the amygdala from thalamic and cortical exteroceptive systems, as well as by subcortical visceral afferent pathways. The neuronal interactions between the amygdala enable the individual to initiate adaptive behaviors to threat based upon the nature of the threat and prior experience. The efferent pathways involving the amygdala, locus coeruleus, hypothalamus, periaqueductal gray, and striatum mediate autonomic, neuroendocrine, and skeletal-motor responses associated with fear and anxiety. The proposed brain structures, neural mechanisms, and neural circuits related to anxiety provide a basis for increased understanding of the pathophysiology of anxiety disorders.
Afferent Pathways↗
Spinal evoked potential in man: a maturational study.
Summated evoked potentials to peroneal nerve stimulation which arise in the cauda equina and spinal cord afferent pathways were recorded from surface electrodes placed over the spine of 95 infants, children and adults. The conduction velocity of these potentials from lumbar to cervical recording sites was calculated. Additionally, segmental conduction velocities over peroneal nerve, caudal and rostral spinal cord were determined. In all age groups the speed of conduction up the spine was non-linear. It was slower over caudal spinal cord segments than over peripheral nerve or rostral cord. All these velocities were about half adult values in the newborn and progressively increased with age. The conduction velocity over peripheral nerve was within the adult range by 3 years of age. The speed of conduction over the spinal cord did not reach adult values until the 5th year. This suggests that spinal cord afferent pathways mature at a slower rate than peripheral nerve fibers.
Adolescent↗
Afferent mechanisms of acute responses of renal sympathetic nerve activity to microgravity.
Exposure to microgravity is thought to induce an alteration of autonomic function through several afferent pathways. First, a removal of all hydrostatic gradients, which results in a large cephalad fluid shift. The fluid shift may induce an increase in transmural pressure in the cardiopulmonary region, which stimulates cardiopulmonary mechanoreceptors and baroreceptors, and elicits neurogenic responses. Secondly, an alteration of the vestibular input may modify sympathetic output via the vestibulosympathetic reflex. However, there is a lack of direct evidence for the role of cardiopulmonary mechanoreceptors, baroreceptors, and vestibular system in autonomic responses to microgravity. Accordingly, responses of renal sympathetic nerve activity (RNA) to microgravity, produced by free drop, were examined in anesthetized rats. To examine the afferent pathways of the RNA responses, the same experiment was performed in rats that had undergone labyrinthectomy, sinoaortic baroreceptor denervation (SAD), vagotomy, or SAD plus vagotomy.
Afferent Pathways↗
Responses of neurons in rostral ventrolateral medulla to activation of cardiac receptors in rats.
Ischemic stimulation of cardiac receptors reflexly excites the cardiovascular system. However, the supraspinal mechanisms involved in this reflex are not well defined. This study examined the responses of barosensitive neurons in the rostral ventrolateral medulla (RVLM) to stimulation of cardiac receptors and the afferent pathways involved in these responses. Single-unit activity of RVLM neurons was recorded in alpha-chloralose-anesthetized rats. Cardiac receptors were stimulated by epicardial application of 10 microg/ml of bradykinin (BK). Barosensitive neurons were silenced by stimulation of baroreceptors. Application of BK increased the mean arterial pressure from 65.2 +/- 1.9 to 89.3 +/- 2.9 mmHg and excited RVLM barosensitive neurons from 6.2 +/- 0.7 to 10.7 +/- 0.9 impulses/s (P < 0.05, n = 40). BK had no effect on 21 nonbarosensitive neurons. Blockade of stellate ganglia abolished the response of barosensitive neurons to BK. Cervical vagotomy significantly increased the baseline discharges of RVLM barosensitive neurons but had no effect on their responses to BK. Thus this study indicates that stimulation of cardiac receptors selectively activates RVLM barosensitive neurons through sympathetic afferent pathways. This information suggests that the RVLM barosensitive neurons are likely involved in the sympathetic control of circulation during myocardial ischemia.
Afferent Pathways↗
Custom-designed high-density conformal planar multielectrode arrays for brain slice electrophysiology.
Multielectrode arrays have enabled electrophysiological experiments exploring spatio-temporal dynamics previously unattainable with single electrode recordings. The finite number of electrodes in planar MEAs (pMEAs), however, imposes a trade-off between the spatial resolution and the recording area. This limitation was circumvented in this paper through the custom design of experiment-specific tissue-conformal high-density pMEAs (cMEAs). Four configurations were presented as examples of cMEAs designed for specific stimulation and recording experiments in acute hippocampal slices. These cMEAs conformed in designs to the slice cytoarchitecture whereas their high-density provided high spatial resolution for selective stimulation of afferent pathways and current source density (CSD) analysis. The cMEAs have 50 or 60 microm center-to-center inter-electrode distances and were manufactured on glass substrates by photolithographically defining ITO leads, insulating them with silicon nitride and SU-8 2000 epoxy-based photoresist and coating the etched electrode tips with gold or platinum. The ability of these cMEAs to stimulate and record electrophysiological activity was demonstrated by recording monosynaptic, disynaptic, and trisynaptic field potentials. The conformal designs also facilitated the selection of the optimal electrode locations for stimulation of specific afferent pathways (Schaffer collaterals; medial versus lateral perforant path) and recording the corresponding responses. In addition, the high-density of the arrays enabled CSD analysis of laminar profiles obtained through sequential stimulation along the CA1 pyramidal tree.
Afferent Pathways↗
Secondary cervical dystonia associated with structural lesions of the central nervous system.
We tested the hypothesis that structural lesions of the central nervous system (CNS) associated with cervical dystonia more commonly involve the cerebellum and its primary afferent pathways than basal ganglia structures. Cervical dystonia is the most common focal dystonia, the majority of cases are idiopathic, and only a small percentage of patients have a family history of dystonia or other movement disorders. Pathophysiological mechanisms operative in solely or predominantly appendicular dystonias such as writer's cramp and Oppenheim's dystonia, respectively, may not be directly applicable to axial dystonias. The localization of structural lesions of the CNS associated with secondary cervical dystonia may provide some insight into the neural structures potentially involved in primary cervical dystonia. The National Library of Medicine Gateway (from 1960) and a clinical database maintained by the senior author (from 1999) were searched for cases of secondary cervical dystonia associated with structural lesions of the CNS. Search terms included one or more of the following: dystonia, torticollis, cervical, secondary, and symptomatic. Lesion localization and type, patient age, patient gender, head position, occurrence of sensory tricks, and associated neurological findings were tabulated for each case. Structural lesions associated with cervical dystonia were most commonly localized to the brainstem and cerebellum. The remaining cases were equally divided between the cervical spinal cord and basal ganglia. Although inconsistent, head rotation tended to be contralateral to lesion localization. Additional neurological abnormalities were present in the majority of patients with secondary cervical dystonia. The relative paucity of basal ganglia pathology and concentration of lesions in the brainstem, cerebellum, and cervical spinal cord in patients with secondary cervical dystonia suggests that dysfunction of cerebellar afferent pathways may be important to the pathophysiology of primary cervical dystonia.
Adult↗
Motor neuron disease with multi-system involvement presenting as tetraparesis, ophthalmoplegia and sensori-autonomic dysfunction.
We carried out a postmortem examination on two Japanese patients, 64- and 80-year-old men whose survival was prolonged with an artificial respirator. They had no family history of neuropsychiatric disorders and were suspected, clinically, as having a motor neuron disease that differed from amyotrophic lateral sclerosis (ALS). As well as upper and lower motor neuron impairment, they showed a variety of symptoms, such as sensory disturbances, hypohidrosis, impotence, ophthalmoparesis and/or atonic neurogenic bladder, and their protein content in cerebrospinal fluid was elevated markedly. Pathological examination revealed the following extensive nervous system involvement: (1) the upper and lower voluntary motor systems, including the IIIrd, IVth and VIth cranial nerve nuclei: (2) the reticular formation and its major afferent pathways; (3) the vestibulospinal and tectospinal systems; (4) the spinocerebellar system and the exteroceptive somatic afferent pathways; (5) the dentatorubral and pallidoluysian systems; and (6) the substantia nigra, locus ceruleus and intermediolateral and Onufrowicz's nuclei. Neither Bunina bodies, Lewy body-like hyaline inclusions nor ubiquitin immunoreactive skein-like structures were observed. The distribution of the lesions was quite different from that in patients with ALS and the other known related diseases. Recently, seven autopsied cases with clinical and histopathological similarities to our patients have been reported in Japan. Our conclusion is that our two and these seven patients should be classified as having a new motor neuron disease entity, which can be is differentiated from ALS.
Aged↗
Effect of bilateral vagosympathetic nerve blockade on response of the dog upper esophageal sphincter (UES) to intraesophageal distention and acid.
The present study in dogs was performed to elucidate (a) the upper esophageal sphincter responses to intraesophageal distention and acid perfusion and (b) the effect of bilateral nerve blockade on these responses. Balloon distention (5-40 cm3) at 5, 10, 15, and 20 cm below the sphincter produced up to a 400% increase in sphincter pressure. The threshold for this response increased, and the maximum sphincter response decreased as distention was performed more distally in the esophagus. Perfusion of acid (0.1-0.4 N HCl) at the level of the upper esophageal sphincter and at 5, 10, and 15 cm below, produced a similar increase in sphincter pressure. The maximum response to acid occurred on perfusion at the sphincter and the response decreased progressively with perfusion distally. Bilateral nerve blockade produced (a) no change in resting sphincter pressure or in the sphincter response to swallowing, (b) a partial reduction in the maximum sphincter response to distention, and (c) abolition of the response to acid. A significant portion of the afferent pathway for the response of the upper esophageal sphincter to distention and virtually all the afferent pathways for the response to acid are carried in the vagosympathetic trunks presumably via the recurrent laryngeal nerves.
Animals↗
Suppression of detrusor-sphincter dyssynergia by immunoneutralization of nerve growth factor in lumbosacral spinal cord in spinal cord injured rats.
PURPOSE: We investigated the effects of intrathecal application of nerve growth factor (NGF) antibodies (NGF-Abs) and desensitization of C-fiber afferent pathways by capsaicin treatment on detrusor-sphincter dyssynergia (DSD) after spinal cord injury (SCI). MATERIALS AND METHODS: In adult female rats SCI was induced by complete transection of the spinal cord at Th8 to 9. Ten days after spinalization vehicle or NGF-Ab (10 microg daily) was continuously administered at the level of the L6-S1 spinal cord through an implanted intrathecal catheter connected to an osmotic pump for 2 weeks. Another group of spinalized rats was treated with capsaicin (125 mg/kg subcutaneously) 3 weeks after spinalization and 5 days before experiments. Simultaneous recordings of intravesical pressure and urethral perfusion pressure were then performed. NGF levels in the L6 spinal cord were measured in vehicle or NGF-Ab treated spinalized rats using enzyme-linked immunosorbent assay. RESULTS: DSD was observed in all vehicle treated spinalized rats. The average urethral pressure increase at the peak bladder contraction was significantly lower by 84% and 78% in NGF-Ab and capsaicin treated spinalized rats, respectively, than in vehicle treated rats. After NGF-Ab treatment NGF levels were significantly decreased by 38% in the L6 spinal cord compared with vehicle treated spinalized rats, in which NGF levels in the L6 spinal cord were 7 times higher than in spinal intact rats. CONCLUSIONS: Increased levels of NGF in the spinal cord could contribute to the emergence of DSD that is at least in part mediated by C-fiber bladder afferents after SCI. Thus suppression of NGF levels in afferent pathways could be useful for treating DSD following SCI.
Afferent Pathways↗
Is the hyperpnea of muscular contractions critically dependent on spinal afferents?
We studied the role of spinal afferent pathways in the hyperpnea of electrically induced muscle contractions (ExE). The ventilatory (VE) and arterial CO2 partial pressure (PaCO2) responses were measured at rest and during two levels of ExE in awake human paraplegic subjects with clinically complete lesions of the spinal cord (range T4-T11). We hypothesized that if peripheral neural drive is critical to a normal ventilatory response, then ExE in the absence of intact pathways should cause a lower ventilatory response resulting in hypercapnia at the onset of ExE. ExE was induced by stimulation of the quadriceps and hamstring muscles that approximately doubled the resting level of CO2 production (VCO2). PaCO2 during work transitions and in the latter stages of ExE did not differ significantly from that at rest. Arterial pH progressively declined over time during ExE (P less than 0.01) as a result of increased lactate concentration (P less than 0.01). The linear relationship between VE and VCO2 was similar to that found for normal human subjects during ExE (P = 0.73). These data suggest that VE and presumably alveolar ventilation (VA) can be appropriately matched to VCO2 during low-intensity muscle contractions of the lower extremities in the absence of intact spinal afferent pathways. Moreover, since it is unlikely that postulated "central command" mechanisms were initiated during ExE in these paraplegic subjects, the data provide support for our previous conclusion that central command is not obligatory for matching VA to VCO2 (J. Appl. Physiol. 64: 218-225, 1988).
Adult↗