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Efferent Fibers (efferent + fiber)
Selected AbstractsTerminal nerve and visionMICROSCOPY RESEARCH AND TECHNIQUE, Issue 1-2 2004U. Behrens Abstract The vertebrate retina receives efferent input from different parts of the central nervous system. Efferent fibers are thought to influence retinal information processing but their functional role is not well understood. One of the best-described retinopetal fiber systems in teleost retinae belongs to the terminal nerve complex. Gonadotropin-releasing hormone (GnRH) and molluscan cardioexcitatory tetrapeptide (FMRFamide)-containing fibers from the ganglion of the terminal nerve form a dense fiber plexus in the retina at the border of the inner nuclear and inner plexiform layer. Peptide-containing fibers surround and contact perikarya of dopaminergic interplexiform cells in teleost retina. In vitro experiments demonstrated that exogenously supplied GnRH mediates dopaminergic effects on the membrane potential and on the morphology of dendritic tips (spinules) of cone horizontal cells. These effects can be specifically blocked by GnRH-antagonists, indicating that the release of dopamine and dopamine-dependent effects on light adaptation of retinal neurons are affected by the terminal nerve complex. Recent data have shown that olfactory information has an impact on retinal physiology, but its precise role is not clear. The efferent fiber of the terminal nerve complex is one of the first retinopetal fiber systems for which the sources of the fibers, their cellular targets, and several physiological, morphological, and behavioral effects are known. The terminal nerve complex is therefore a model system for the analysis of local information processing which is influenced by a distinct fiber projection. Microsc. Res. Tech. 65:25,32, 2004. © 2004 Wiley-Liss, Inc. [source] The intestinal barrier and its regulation by neuroimmune factorsNEUROGASTROENTEROLOGY & MOTILITY, Issue 7 2010å. v. Keita Abstract Background, The ability to control uptake across the mucosa and protect from damage of harmful substances from the lumen is defined as intestinal barrier function. A disturbed barrier dysfunction has been described in many human diseases and animal models, for example, inflammatory bowel disease, irritable bowel syndrome, and intestinal hypersensitivity. In most diseases and models, alterations are seen both of the paracellular pathway, via the tight junctions, and of the transcellular routes, via different types of endocytosis. Recent studies of pathogenic mechanisms have demonstrated the important role of neuroimmune interaction with the epithelial cells in the regulation of barrier function. Neural impulses from extrinsic vagal and/or sympathetic efferent fibers or intrinsic enteric nerves influence mucosal barrier function via direct effects on epithelial cells or via interaction with immune cells. For example, by nerve-mediated activation by corticotropin-releasing hormone or cholinergic pathways, mucosal mast cells release a range of mediators with effects on transcellular, and/or paracellular permeability (for example, tryptase, TNF-,, nerve growth factor, and interleukins). Purpose, In this review, we discuss current physiological and pathophysiological aspects of the intestinal barrier and, in particular, its regulation by neuroimmune factors. [source] Voiding reflex in chronic spinal cord injured cats induced by stimulating and blocking pudendal nerves,,NEUROUROLOGY AND URODYNAMICS, Issue 6 2007Changfeng Tai Abstract Aims To induce efficient voiding in chronic spinal cord injured (SCI) cats. Methods Voiding reflexes induced by bladder distension or by electrical stimulation and block of pudendal nerves were investigated in chronic SCI cats under ,-chloralose anesthesia. Results The voiding efficiency in chronic SCI cats induced by bladder distension was very poor compared to that in spinal intact cats (7.3,±,0.9% vs. 93.6,±,2.0%, P,<,0.05). In chronic SCI cats continuous stimulation of the pudendal nerve on one side at 20 Hz induced large amplitude bladder contractions, but failed to induce voiding. However, continuous pudendal nerve stimulation (20 Hz) combined with high-frequency (10 kHz) distal blockade of the ipsilateral pudendal nerve elicited efficient (73.2,±,10.7%) voiding. Blocking the pudendal nerves bilaterally produced voiding efficiency (82.5,±,4.8%) comparable to the efficiency during voidings induced by bladder distension in spinal intact cats, indicating that the external urethral sphincter (EUS) contraction was caused not only by direct activation of the pudendal efferent fibers, but also by spinal reflex activation of the EUS through the contralateral pudendal nerve. The maximal bladder pressure and average flow rate induced by stimulation and bilateral pudendal nerve block in chronic SCI cats were also comparable to those in spinal intact cats. Conclusions This study shows that after the spinal cord is chronically isolated from the pontine micturition center, bladder distension evokes a transient, inefficient voiding reflex, whereas stimulation of somatic afferent fibers evokes a strong, long duration, spinal bladder reflex that elicits efficient voiding when combined with blockade of somatic efferent fibers in the pudendal nerves. Neurourol. Urodynam. 26:879,886, 2007. © 2007 Wiley-Liss, Inc. [source] Guanosine-Induced Synaptogenesis in the Adult Brain In VivoTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 12 2009Inmaculada Gerrikagoitia Abstract Astrocytes release factors like cholesterol, apoE, and pleiotropic molecules that influence synaptogenesis in the central nervous system. In vitro studies have shown that guanosine elicits the production and further release of these synaptogenic factors. To demonstrate that such astrocytic factors are synaptogenic in vivo, osmotic pumps were implanted in primary visual cortex (VC) of Sprague-Dawley rats to deliver guanosine. Simultaneous injection of dextran amine as an anterograde tracer at the same site where the osmotic pumps were implanted enabled the morphology of the fibers emerging from the VC to be visualized as well. The guanosine-treated efferent connections from these animals showed a significant increase in the number and size of synaptic boutons along the efferent fibers when compared with controls. A similar increase in the number and size of synaptic boutons was also detected when the cortico,cortical connection to the lateral secondary visual area was studied in more detail. The ensuing morphological changes to the synapses did not show a clear preference for any particular type or site of the axonal branches that integrates this cortical connection. Moreover, the distribution of boutons along the fibers was clearly stochastic according to their size. Thus, guanosine administration appears to open up the possibility of manipulating connections to compensate for total or partial denervation. Anat Rec, 292:1968,1975, 2009. © 2009 Wiley-Liss, Inc. [source] Phrenic paresis,a possible additional spinal cord dysfunction induced by neck manipulation in cervical spondylotic myelopathy (CSM): A report of two cases with anatomical and clinical considerationsCLINICAL ANATOMY, Issue 3 2001Wesley W. Parke Abstract The clinical records of two male subjects with severe cervical spondylotic myelopathy (CSM) who developed respiratory insufficiency after the cervical manipulation involved in preoperative anesthetic intubation were examined. Their cervical imaging was analyzed with respect to the known anatomic relationships of the spinal phrenic nerve nuclei to the spondylotic compressive lesions in an attempt to provide the anatomic and pathologic rationales that may explain this phrenic paresis as a possible traumatic complication of severe CSM. Perusal of extant literature revealed extensive descriptions of CSM symptoms, but none had previously reported an associated neuromuscular weakness of the diaphragm. Magnetic resonance imaging analyses indicated that the existing degree of upper cervical cord compression, when reinforced by the additional posterior and anterior pressures consequent to cervical spinal extension and flexion, could readily account for the functional impairment of phrenic nerve neuron cells and/or their efferent fibers. Thus, the anatomic relations of the phrenic nerve nuclear columns and their efferent tracts predispose them to interference by compressive lesions found in CSM, and undue manipulation of the cervical spine when advanced stenosis is known to be present should be recognized as a possible cause of cervical spondylotic myelopathic,phrenic paresis. Clin. Anat. 1:173,178, 2001. © 2001 Wiley-Liss, Inc. [source] | |||||||||||||