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PubMed1987

Relative afferent pupillary defect in a lesion of the pretectal afferent pupillary pathway.

A 23-year-old man presented with Parinaud's syndrome due to a mixed germ cell tumour of the pineal gland. Following treatment the syndrome resolved, but the patient was noted to have a relative afferent pupillary defect (RAPD) without any detectable visual dysfunction. The authors localize the lesion to the pretectal afferent pupillary pathway and discuss the differential diagnosis of an RAPD in the presence of normal visual function.

Adult↗
PubMed1994

Suppression of motor cortical excitability by electrical stimulation over the cerebellum in ataxia.

We studied the effect of electrical stimulation over the cerebellum on electromyographic responses evoked by magnetic stimulation over the cerebral motor cortex in 41 normal volunteers and 32 patients with ataxia due to various disorders. In all the normal subjects, stimulation over the cerebellum significantly reduced the size of electromyographic response in the first dorsal interosseous muscle evoked by magnetic cortical stimulation, when the cerebellar stimulus preceded the cortical stimulus by 5, 6, and 7 msec. This suppression was absent or reduced in ataxic patients who had atrophy of the cerebellar hemispheres as demonstrated by magnetic resonance imaging and in patients with dysfunction of the cerebellothalamocortical pathway who had lesions in the superior cerebellar peduncle or in the motor thalamus. In contrast, suppression was normal in ataxic patients who had pontine lesions that affected the pontocerebellar afferent pathway to the cerebellum. Results were also normal in patients without cerebellar ataxia, such as those with Parkinson's disease, sensory ataxia, and cerebrovascular disease without ataxia. We conclude that electrical stimulation activates cerebellar structures that suppress motor cortical excitability through a cerebellothalamocortical pathway and that the afferent systems to the cerebellum make no or little contribution to the effect. The technique described here would be useful for distinguishing ataxia due to lesions of cerebellar afferent pathway from other types of cerebellar ataxia.

Adult↗
PubMed1985

The hepatic vagus nerve and the neural regulation of insulin secretion.

Despite considerable evidence that vagal neural efferent pathways between brainstem and pancreatic islets may alter the secretion of insulin, afferent pathways which might affect this system have received little attention. In the present work we have examined the effects on plasma insulin concentration of several treatments designed to alter the neural activity of the hepatic vagus nerve, a major afferent pathway between the liver and the medulla. The hepatic vagus nerve was acutely sectioned or stimulated electrically in separate experiments in rats. In a third experiment, glucose or 3-O-methylglucose was given ip to stimulate or inhibit, respectively, the hypothetical hepatic glucoreceptors. The effects of these treatments were assessed by measuring arterial or portal plasma insulin concentrations. Anesthesia and its possible secondary inhibitory effects on insulin secretion were avoided by a spinal sectioning of the rats in the cervical region, before experimentation. Acute section of the hepatic vagus nerve between the liver and the main anterior vagal trunk caused an increase in both arterial and portal plasma insulin concentrations. Stimulation of the central end of the nerve suppressed the concentration of the hormone in both the arterial and portal plasma relative to sham-stimulated controls. Section of the celiac vagal branches to the pancreas abolished these changes. Intraperitoneal glucose enhanced arterial insulin more in sham-vagotomized than in hepatic-vagotomized rats. After 3-O-methylglucose was given ip, the response was the opposite: insulin rose more in the arterial plasma of the hepatic-vagotomized animals than in those sham vagotomized. These results suggest that the hepatic vagus nerve plays a role in the regulation of insulin secretion. They are consistent with the hypothesis that afferent fibers in this nerve exert a tonic inhibition on the brainstem centers of an efferent vagal pancreatic neuroendocrine system.

3-O-Methylglucose↗
PubMed2006

Mutations in the gene encoding pejvakin, a newly identified protein of the afferent auditory pathway, cause DFNB59 auditory neuropathy.

Auditory neuropathy is a particular type of hearing impairment in which neural transmission of the auditory signal is impaired, while cochlear outer hair cells remain functional. Here we report on DFNB59, a newly identified gene on chromosome 2q31.1-q31.3 mutated in four families segregating autosomal recessive auditory neuropathy. DFNB59 encodes pejvakin, a 352-residue protein. Pejvakin is a paralog of DFNA5, a protein of unknown function also involved in deafness. By immunohistofluorescence, pejvakin is detected in the cell bodies of neurons of the afferent auditory pathway. Furthermore, Dfnb59 knock-in mice, homozygous for the R183W variant identified in one DFNB59 family, show abnormal auditory brainstem responses indicative of neuronal dysfunction along the auditory pathway. Unlike previously described sensorineural deafness genes, all of which underlie cochlear cell pathologies, DFNB59 is the first human gene implicated in nonsyndromic deafness due to a neuronal defect.

Amino Acid Sequence↗
PubMed2000

NADPH-diaphorase reveals presumptive sympathetic primary afferents in the developing human spinal cord.

Numerous studies have elucidated two visceral afferent pathways in the spinal cord of mammals, the lateral collateral pathway (LCP) and the medial collateral pathway (MCP). The present study utilized NADPH-diaphorase histochemistry to visualize afferent pathways in the developing human thoracolumbar spinal cord. Diaphorase-positive fiber bundles, strikingly similar to the previously defined LCP and MCP, were observed coursing along the lateral and medial aspects of the dorsal horn to the base of the dorsal horn, the intermediate gray, and/or the dorsal commissure. Furthermore, some axons forming the MCP crossed in the dorsal commissure to the contralateral side of the spinal cord. In addition, axons projecting in the LCP often appeared to terminate within clusters of diaphorase-labeled sympathetic preganglionic neurons, supporting the concept that monosynaptic connections may exist between primary afferents and autonomic motor neurons. Thus, nitric oxide may be involved in both afferent and efferent neurons in reflex pathways of the human sympathetic nervous system.

Adrenergic Fibers↗
PubMed2000

Leptin injection into white adipose tissue elevates renal sympathetic nerve activity dose-dependently through the afferent nerves pathway in rats.

Recent studies suggested that leptin in white adipose tissue (WAT) affected the sympathetic out flow to several tissues. We examined whether elevations of renal sympathetic nerve activity (RSNA) and blood pressure (BP) could be observed by leptin injection into WAT in rats. Injections of leptin (10 and 100 ng/ml per kg) into WAT evoked the activation of RSNA dose-dependently. Circulating sympathetic nerve activators, such as leptin, insulin, glucose and lactate, were unchanged by any doses of leptin. In addition, BP was not affected by leptin injections during a 90 min experimental period. These data suggested that leptin activated the afferent nerves through the sensors in WAT, resulting in elevation of RSNA.

Adipose Tissue↗
PubMed2006

Neurophysiological evaluation of healthy human anorectal sensation.

Patients with functional gastrointestinal disorders often demonstrate abnormal visceral sensation. Currently, rectal sensation is assessed by manual balloon distension or barostat. However, neither test is adaptable for use in the neurophysiological characterization of visceral afferent pathways by sensory evoked potentials. The aim of this study was to assess the reproducibility and quality of sensation evoked by electrical stimulation (ES) and rapid balloon distension (RBD) in the anorectum and to apply the optimum stimulus to examine the visceral afferent pathway with rectal evoked potentials. Healthy subjects (n = 8, median age 33 yr) were studied on three separate occasions. Variability, tolerance, and stimulus characteristics were assessed with each technique. Overall ES consistently invoked pain and was chosen for measuring rectal evoked potential whereas RBD in all cases induced the strong urge to defecate. Rectal intraclass correlation coefficient (ICC) for ES and RBD (0.82 and 0.72, respectively) demonstrated good reproducibility at pain/maximum tolerated volume but not at sensory threshold. Only sphincter ICC for ES at pain showed acceptable between-study reproducibility (ICC 0.79). Within studies ICC was good (>0.6) for anorectal ES and RBD at both levels of sensation. All subjects reported significantly more unpleasantness during RBD than ES (P < 0.01). This study demonstrates that ES and RBD are similarly reproducible. However, the sensations experienced with each technique differed markedly, probably reflecting differences in peripheral and/or central processing of the sensory input. This is of relevance in interpreting findings of neuroimaging studies of anorectal sensation and may provide insight into the physiological characteristics of visceral afferent pathways in health and disease.

Adolescent↗
PubMed2006

Targeted disruption of the murine CCK1 receptor gene reduces intestinal lipid-induced feedback inhibition of gastric function.

Cholecystokinin (CCK), acting at CCK1 receptors (CCK1Rs) on intestinal vagal afferent terminals, has been implicated in the control of gastrointestinal function and food intake. Using CCK1R(-/-) mice, we tested the hypothesis that lipid-induced activation of the vagal afferent pathway and intestinal feedback of gastric function is CCK1R dependent. In anesthetized CCK1R(+/+) ("wild type") mice, meal-stimulated gastric acid secretion was inhibited by intestinal lipid infusion; this was abolished in CCK1R(-/-) mice. Gastric emptying of whole egg, measured by nuclear scintigraphy in awake mice, was significantly faster in CCK1R(-/-) than CCK1R(+/+) mice. Gastric emptying of chow was significantly slowed in response to administration of CCK-8 (22 pmol) in CCK1R(+/+) but not CCK1R(-/-) mice. Activation of the vagal afferent pathway was measured by immunohistochemical localization of Fos protein in the nucleus of the solitary tract (NTS; a region where vagal afferents terminate). CCK-8 (22 pmol ip) increased neuronal Fos expression in the NTS of fasted CCK1R(+/+) mice; CCK-induced Fos expression was reduced by 97% in CCK1R(-/-) compared with CCK1R(+/+) mice. Intralipid (0.2 ml of 20% Intralipid and 0.04 g lipid), but not saline, gavage increased Fos expression in the NTS of fasted CCK1R(+/+) mice; lipid-induced Fos expression was decreased by 47% in CCK1R(-/-) compared with CCK1R(+/+)mice. We conclude that intestinal lipid activates the vagal afferent pathway, decreases gastric acid secretion, and delays gastric emptying via a CCK1R-dependent mechanism. Thus, despite a relatively normal phenotype, intestinal feedback in response to lipid is severely impaired in these mice.

Animals↗
PubMed1985

Vasopressin secretion in progressive autonomic failure: evidence for defective afferent cardiovascular pathways.

Patients with progressive autonomic failure with multiple system atrophy show a severely blunted response of plasma arginine vasopressin to the stimulus of head-up tilt. Whether this could be due to lesions either at one or more sites within ascending neural pathways from cardiovascular stretch receptors in the thorax or, alternatively, to lesions affecting vasopressin secreting cells within the hypothalamus was investigated. The arginine vasopressin response to an intravenous infusion of hypertonic saline was determined in six patients with progressive autonomic failure. The mean plasma concentration of arginine vasopressin rose from 1.0 to 3.7 pmol/l, a change comparable to that observed in normal controls. This demonstrates normal functioning of the efferent connections from the osmoreceptors within the hypothalamus and suggests that the loss of vasopressin response to head-up tilt is due to lesions in ascending pathways from cardiovascular receptors. There was a significant rise in mean blood pressure during the infusions on patients with progressive autonomic failure, a change which was not observed with the controls. This may have been at least partly caused by the rise in circulating arginine vasopressin concentrations, since these patients have been reported to be extremely sensitive to the pressor effects of arginine vasopressin.

Afferent Pathways↗
PubMed1995

Regional zinc staining in postmortem hippocampus from schizophrenic patients.

Schizophrenia-associated deficits in learning and memory have been associated with a decrease in the volume of the hippocampus, but the specific nature of the neuronal deficit remains unknown. Many critical afferent pathways in the hippocampus contain ionic zinc. Alterations of these pathways could be manifest as a decrease in ionic zinc levels within hippocampal afferent pathways. This possibility was examined in postmortem hippocampal tissue taken from schizophrenic patients, patients with other psychiatric disorders and matched, non-mentally ill subjects using a modified Timm's silver staining method. The three groups exhibited similar patterns of zinc staining within the hippocampal formation as well as similar levels of zinc within the mossy fiber projection system. A greater prevalence of zinc staining within the inner molecular layer of the dentate gyrus was observed in female as compared to male donors and in older as compared to younger donors. The results of the present study demonstrate that loss of ionic zinc within the hippocampus does not appear to be part of the pathology of schizophrenia.

Adolescent↗
PubMed1976

Afferent neural pathway in the regulation of cardiopulmonary responses to tissue hypermetabolism.

We studied the role of neural transmission from hypermetabolic peripheral tissues in the regulation of cardiac output and pulmonary ventilation in chloralose-anesthetized dogs. Cross-circulation techniques with femoral-femoral or femoral-aortic anastomoses were used to produce a vascularly isolated, but normally innervated, hindlimb or lower half-body, 2,4-Dinitrophenol (DNP) was infused into the arterial side of the perfusion circuit to triple oxygen consumption and to increase lactate production by the cross-perfused area. After infusion of DNP, cardiac output and mean systemic arterial blood pressure increased, but neither heart rate nor pulmonary artery wedge pressure changed significantly. Pulmonary minute ventilation and arterial pH also increased, while arterial PCO2 fell. These changes were abolished when the nerve connections between the perfused limb and its parent body were severed. Normal saline, when administered in a similar manner, did not increase either ventilation or cardiac output, and simple denervation without previous infusions of DNP also had no effect. These results indicate that there are receptors sensitive to metabolic changes in the tissue, and that neural transmission is an important afferent link in regulating the cardiopulmonary responses to increased tissue metabolism.

Afferent Pathways↗
PubMed2002

Objective evaluation of infraorbital nerve involvement in maxillary lesions by means of the blink reflex.

OBJECTIVE: To objectively evaluate the effects of maxillary lesions on the infraorbital nerve (ION). METHODS: We investigated the latencies (R1, R2) of the blink reflex, stimulating the infraorbital foramen electrically (18 mA, 0.2 millisecond). Twenty-two patients with unilateral maxillary lesions were enrolled. RESULTS: Ten patients showed delayed or absent R1 on the lesion side. Four of 20 patients showed delayed difference in R2 latency. Ten (77%) of 13 patients with lesions along the ION pathway showed an abnormal blink reflex. Only 3 patients demonstrated a normal blink reflex despite a lesion along the pathway of the ION. All patients whose ION pathway was intact showed a normal blink reflex. CONCLUSIONS: These results suggested that lesions along the ION pathway may impair the afferent pathway of the blink reflex. The blink reflex may be valuable to evaluate maxillary lesions objectively. Furthermore, R1 is more effective than R2 in detecting ION defects.

Adult↗
PubMed1991

Convergence from the preoptic area and arcuate nucleus to the median eminence in acupuncture and nonacupuncture point stimulation analgesia.

Lesion of the preoptic area (POA) or medial arcuate nucleus (M-HARN) abolished acupuncture analgesia (AA). Potentials in the median eminence (ME) evoked by stimulation of the acupuncture point (AP) were not affected by lesion of either the POA or M-HARN alone, but were abolished by concurrent lesion of both. No analgesia was produced by stimulation of the POA. Analgesia produced by stimulation of the M-HARN was abolished by lesion of the POA, and the abolished analgesia was restored by concurrent stimulation of the POA and M-HARN, hence POA and M-HARN outputs might converge in the ME to produce AA. Similar convergence from the anterior arcuate nucleus (A-HARN) and POA to the ME was observed in analgesia (NAA) produced by stimulation of a nonacupuncture point (NAP). Two pathways diverged from the lateral hypothalamus in the AA afferent pathway and two from the lateral periaqueductal central gray (L-PAG) in the NAA afferent pathway. POA potentials evoked by stimulation of the AP were reversed by naloxone, and those evoked by stimulation of the AP were reversed by dexamethasone. ACTH sensitive sites were found in both the L-PAG and the anterior hypothalamus.

Acupuncture Analgesia↗
PubMed2002

Bladder afferents and their role in the overactive bladder.

The role of afferent innervation of the bladder in the pathophysiology of urinary incontinence has become the focus of intense interest. In normal health, the afferent pathway is mediated largely by Adelta-fibers, which ultimately send information about the state of bladder fullness to the pontine micturition center via the periaqueductal gray matter. However, after spinal disruption, a different type of afferent pathway emerges, mediated by capsaicin-sensitive C-fibers that drive a spinal segmental reflex pathway, causing neurogenic detrusor overactivity. The common sources of afferent information for either pathway are likely to be afferents from the urothelium, lamina propria, and afferents that originate in the bladder wall. Ultrastructural investigations of the constituent neural elements of these structures contribute to our knowledge of their role in both health and disease and help provide a rational approach to treatment strategies. Evidence of the involvement of capsaicin-sensitive C-fibers in the spinal reflex pathway has been supported by the successful treatment of patients with neurogenic incontinence with intravesical capsaicin or its ultrapotent nonpungent analog, resiniferatoxin. On the other hand, capsaicin has not been shown to be clearly effective in treatment of overactive bladder caused by detrusor overactivity or suprapontine pathology without the emergent C-fiber-mediated reflex. It is hoped that continued investigation of neurotoxins that have the potential to act on afferent innervation will lead to other treatment strategies for bladder disorders and other disorders involving afferent dysfunction.

Afferent Pathways↗
PubMed1991

The pathophysiology of chronic relapsing experimental allergic encephalomyelitis in the Lewis rat.

Electrophysiological studies were performed in Lewis rats with chronic relapsing experimental allergic encephalomyelitis (EAE) induced by inoculation with guinea-pig spinal cord and adjuvants and treatment with low dose cyclosporin A. During clinical episodes there was conduction failure in the central nervous system (CNS), namely the spinal cord dorsal columns, and in the afferent fibres in the peripheral nervous system (PNS). The following observations indicated that the conduction failure was mainly due to demyelination-induced conduction block: (1) rate-dependent conduction block in the CNS and PNS; (2) temporal dispersion due to slowing of PNS conduction; (3) restoration of PNS conduction by cooling; (4) restoration of CNS conduction by ouabain; (5) previously demonstrated histological evidence of primary demyelination in the dorsal columns, dorsal root ganglia and dorsal roots; and (6) the temporal association of restoration of conduction with remyelination. However, it is likely that CNS and PNS axonal degeneration, which occurs in this disease, also contributed to the conduction failure. In clinical remissions there was restoration of conduction in the CNS and PNS which can be explained by ensheathment/remyelination by oligodendrocytes and Schwann cells, respectively. In most rats during clinical episodes the cerebral somatosensory evoked potential was reduced in amplitude and prolonged in latency, which can be accounted for by demyelination and axonal degeneration in the CNS and PNS components of the afferent pathway. In 2 rats with episodes of EAE, however, this potential was markedly increased in amplitude, which might have been due to demyelination-induced conduction block of descending pathways that normally inhibit synaptic transmission in the afferent pathway. In well-established remission there was residual conduction failure in the CNS and PNS which can be mainly accounted for by axonal degeneration.

Animals↗
PubMed1996

Ureteral ligation induces Fos expression in the dorsal horn.

To describe a sympathetic afferent circuit, the left ureter was ligated in anesthetized rats for 1.5-2 h followed by immunocytochemical processing to localize expression of either the immediate early gene (IEG) c-fos or Krox-24 in the spinal cord or dorsal root ganglia (DRG). No IEG expression was detected in DRG. Both Fos and Krox-24 expression was found in the dorsal horn. More Fos immunocytochemically stained cells were found in the dorsal horn both ipsi- and and contralateral to the ligated ureter at spinal segments T10-T13 after ureteral than after either sham ligation or anesthesia control procedures. More Fos stained cells were in the dorsal horn ipsilateral to the ligated ureter than on the contralateral side. The Fos staining patterns in the dorsal horn of ligated and sham-ligated animals were similar with most labeled cells in dorsomedial portions of laminae I and II. In contrast, the Fos staining pattern in the dorsal horn in anesthetized animals (unoperated controls) was noticeably different from operated animals with the most Fos cells in the ventrolateral part of laminae I-II. These results indicate that (1) Fos Immunocytochemistry may be useful for tracing sympathetic afferent pathways, (2) the sensory pathway activated by ureteral ligation enters the spinal cord at lower thoracic levels, where renal and upper ureteral afferents are terminating, and (3) some of this sympathetic afferent pathway is located contralateral to the stimulated kidney. Neurons activated by ureteral ligation in the contralateral dorsal horn may mediate reno-renal reflexes.

Afferent Pathways↗
PubMed1977

Connections of latero-dorsal nucleus of the thalamus. II. Experimental study in Papio papio.

Modifications of the latero-dorsal (L.D.) nucleus of the thalamus have been observed earlier in man in relation to limbic lesion of various etiologies. Our proposal was to determine the role of L.D. in memory disturbances. We attempted to study the connections of L.D. in Papio papio baboon after surgical lesion using silver impregnations as well as traditional techniques. We found three afferent pathways: from the fornix, the posterior cingulate and the parietal cortex (area 7). The most important is the afferent system from the fornix, it terminates in the antero-dorso-medial part of L.D.; the other two afferent pathways have a postero-lateral projection in L.D. The three efferent systems to parietal cortex, cingulate and fornix were not delineated in this study. It was concluded that the antero-dorso-medial portion of L.D. is connected to the limbic system and the ventro-postero-lateral portion integrated into a large parieto-cingulo-parahippocampal circuit to which it is joined by direct and indirect projections with several relays. These connections have important implications, perhaps, in our understanding of memory disturbances.

Afferent Pathways↗