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Results for “Neuronal Connectivity”

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PubMed2004

Inhibitory effect of pain-eliciting transcutaneous electrical stimulation on vibration-induced finger flexion reflex in the human upper limb.

We studied the effects of non-pain transcutaneous electrical stimulation (TES) and pain-eliciting TES on vibration-induced finger flexion reflex (VFR) in 12 healthy volunteers. Tonic finger flexion reflex in the upper limb was induced by the application of vibratory stimulation on the volar side of the middle fingertip in the right hand before and after TES. Non-pain TES or pain-eliciting TES was applied on the skin between the bases of the first and second metacarpals in the right hand dorsal area in a crossover design. Pain-eliciting TES inhibited VFRs significantly (Fisher's PLSD, p <0.01), compared to those of the time-control group during and after TES. VFRs were reduced approximately to 63.8% and 78.6% of prestimulation flexion force during and after pain-eliciting TES, respectively. Nonpain TES did not inhibit VFR. These results suggest that pain-conducting afferent fibers have inhibitory neuronal connection over the ipsilateral reflex circuits of VFR in the upper limb.

Adult↗
PubMed2004

Manganese enhanced magnetic resonance imaging.

Manganese is an essential metal that participates as a co-factor in a number of critical biological functions such as electron transport, detoxification of free radicals, and synthesis of neurotransmitters. Like other heavy metals, high concentrations of manganese are toxic. For example, chronic overexposure to manganese leads to movement disorders. In order to maintain this balance between being an essential participant in enzyme function and being a toxic heavy metal, a rich biology has evolved to transport and store manganese. Paramagnetic forms of manganese ions are potent MRI relaxation agents. Indeed, Mn(2+) was the first contrast agent proposed for use in MRI. Recently, there is renewed interest in combining the strong MRI relaxation effects of Mn(2+) with its unique biology in order to expand the range of information that can be measured by MRI. Manganese Enhanced MRI is being developed to give unique tissue contrast, assess tissue viability, act as a surrogate marker of calcium influx into cells and trace neuronal connections. In this article we review recent work and point out prospects for the future uses of manganese enhanced MRI.

Animals↗
PubMed2004

Traumatic injury to CNS fiber tracts--what are the genes telling us?

In contrast to the peripheral nervous system (PNS) nerve fiber tracts of the adult central nervous system (CNS) cannot spontaneously regenerate in response to lesions. As a result injured individuals suffer from chronically impaired neuronal connections leading to major motor-, sensory- and cognitive deficits. It is generally assumed that combinatorial effects account for this regeneration failure including a growth non-permissive environment within CNS lesion zones as well as incomplete activation of axonal growth programmes. In order to design CNS repair strategies it is, therefore, imperative to address the molecular mechanisms responsible for this abortive growth behaviour by means of large scale screening techniques. This review summarizes the outcome of recent gene expression profiling studies investigating local and remote molecular reactions following CNS axotomy.

Axons↗
PubMed1981

Ontogenetic alterations of the cerebral cortex in rat caused by a diet containing a lipid fraction extracted from yeast (Candida lipolytica) grown on N-alkanes.

Several ontogenetic aspects of the cerebral cortex were studied in rats whose mothers were fed on a diet, the lipid fraction of which was extracted from yeast (Candida lipolytica) grown on N-alkanes, during part of pregnancy and throughout lactation. Measures of the heights of some cortical regions and specific layers, the maturation of mean cell volumes and of the cell/gray coefficient, especially in layers I, IV and VI, show that the diet affects cerebral cortex ontogeny. These effects on brain ontogeny and on intrinsic and extrinsic neuron connections may explain the electrophysiological and behavioural alterations observed in previous studies.

Alkanes↗
PubMed1994

Amnesia syndrome following left anterior thalamic infarction; with intrahemispheric and crossed cerebro-cerebellar diaschisis on brain SPECT.

We report a 61-year-old right-handed man developing disturbance of memory after a discrete thalamic infarction. Neuropsychological assessment revealed deficits in memory with retrograde and anterograde components, especially for verbal material. Brain MRI showed a left anterior thalamic infarction with normal angiographic findings. Despite the small lesion in the thalamus, he showed prolonged memory disturbance and a Brain SPECT image revealed decreased uptake in the ipsilateral fronto-temporo-parietal cortex and contralateral cerebellum. This diaschisis, a phenomenon caused by disconnection of the neural pathway helped us to evaluate the functional state of the patient and this imaging technique was valuable for obtaining to get more information for the evaluation of the neurological state and neuronal connections. In conclusion our findings correspond well with the understanding of amnesia as a disconnection syndrome because of the evidence of diaschisis on the Brain SPECT image.

Amnesia↗
PubMedDate not supplied

Motion aftereffect transfer in the monofixation syndrome.

If one adapts to a moving repetitive stimulus of stripes that is suddenly stopped, the stripes will appear to move backward. This apparent backward motion is the motion aftereffect (MAE), and its duration is a measure of its magnitude. If one eye adapts to the moving stimulus and the other eye experiences the aftereffect to the stationary stimulus, the aftereffect has been transferred from one eye to the other and is termed the interocular transfer of the MAE. Experimental evidence indicates that the degree of MAE transfer correlates with clinical binocularity. This study compares the MAE transfer in six subjects with the monofixation syndrome to five normal subjects. The stimuli used are sinusoidal stripes generated on two cathode-ray tubes, subtending either 8 degrees or 2 degrees of visual angle with a periodicity of either 0.5 or 3 cycles/degree presented haploscopically. Subjects with the monofixation syndrome differed significantly from normal subjects in the amount of MAE transferred, implying a lack of central neuronal connections in addition to those mediating conscious central fusion in clinical sensory testing.

Adaptation, Physiological↗
PubMedDate not supplied

Neural misdirection in congenital ocular fibrosis syndrome: implications and pathogenesis.

A child with congenital ocular fibrosis syndrome and oculocutaneous albinism displayed two distinct neural misdirection syndromes: synergistic divergence and Marcus Gunn jaw winking. This and other reported cases of misdirected innervation in patients with congenital fibrosis syndrome suggest that normal neuronal connections fail to become established early in development and that lack of innervation may underlie the pathologic features of the disorder. The prevailing concept of congenital fibrosis syndrome as a primary myopathy should be reconsidered.

Albinism↗
PubMed1999

[Role of vesicle fusion mechanism and cell adhesion molecules in growth cone elongation and synaptogenesis].

Growth cones have been regarded to play central roles in forming complex neural network through target tract selection and target cell recognition. We have found that the vesicle fusion molecular system in growth cones is similar to that in synapses. The cleavage of SNAP25, a protein involved in neurotransmitter release in synapse, resulted in inhibition of neurite elongation. Inversely the overexpression of VAMP2/synaptobrevin, another protein involved in neurotransmitter release in synapse, in PC12 cells resulted in promotion of neurite elongation. We have recently isolated a novel components at cadherin-based cell-cell adherens junctions, named neurabin I, neurabin II, and afadin. Neurabin I is specifically expressed in nervous tissues and localized at synapses. Afadin is uviquitously expressed in various tissues and highly concentrated at cell-cell adherens junctions of small intestine epithelial cells, cardiac muscles, synapses. We have identified the transmembrane protein binding to afadin, and named it nectin, which belongs to immunoglobulin superfamily. Nectin, afadin, neurabin I, and neurabin II may be key molecules to find out various unknown guidance cues which can induce regenerating growth cones to repair the functional neuronal connections in central nervous system after injury.

Animals↗
PubMed1999

Identification of neural projections from the forebrain to the kidney, using the virus pseudorabies.

These data demonstrate a chain of synaptically connected neurons extending to the rat kidney through several levels of the neuraxis from the forebrain, and the lamina terminalis -- an area known to be involved in the regulation of body fluid homeostasis. The Bartha strain of pseudorabies virus was injected into the kidney of male Sprague-Dawley rats, resulting in retrograde infections in spinal cord segments (T1-T8), and successive infection in five autonomic 'premotor' areas of the brain, the rostroventrolateral medulla, rostroventromedial medulla, raphe nuclei, A5 region of the pons, and the paraventricular nucleus of the hypothalamus, as well as the nucleus of the solitary tract, locus coeruleus, and subcoeruleus nuclei. Higher order labelling was found in regions of the forebrain, including the organum vasculosum of the lamina terminalis, median preoptic nucleus, subfornical organ, medial preoptic area, bed nucleus of the stria terminalis, anteroventral periventricular nucleus, lateral preoptic area, suprachiasmatic nucleus, retrochiasmatic nucleus, primary motor cortex, and visceral cortex. This polysynaptic pathway to the kidney may form the substrate underlying the impact of forebrain structures on renal function.

Animals↗
PubMed2000

[Pathophysiology of pain].

Progress in the knowledge of the pathophysiology of pain allow to associate clinical symptoms of painful syndroms to physiological, morphological and neurobiochemical changes observed both at peripheral and central sites. Thus, nociceptive pains involve both a sensitisation of nociceptors and a secondary central sensitisation. Numerous mediators are involved in these phenomena which reflect neuroplasticity. Peripherally, they come from plasma, immune cells and afferent fibres involved in neurogenic inflammation. Their number explains how the peripheral mechanisms of pain are complex and how it is difficult to pharmacologically suppress the activity of nociceptors. Other mediators are involved in the dorsal horn of the spinal cord. Excitatory amino acids are particularly involved by acting on NMDA receptors; substance P seems to work as a facilitatory neuromodulator rather than as a neurotransmitter. The mechanisms of neuropathic pains are different because both small and large diameter afferent fibers are involved. Ectopic discharges from lesional sites of C fibers, sprouting and abnormal neuronal connections have been described. Up regulation of ionic, especially sodic, channels has been demonstrated and could explain spontaneous discharges. Here again, central sensitisation is also observed but present knowledge does not allow to distinguish specific mechanisms. These progress in the knowledge of pathophysiology of pain allow to improve the understanding of the mechanism of action of analgesic drugs. They also give basis to the discovery of novel drugs with original mechanisms.

Humans↗
PubMed2000

Interaction of the Bezold-Jarisch reflex with the urinary bladder function.

OBJECTIVES: The Bezold-Jarisch reflex involves a marked increase in vagal (parasympathetic) efferent discharge to the heart. During micturition, there is a marked increase in parasympathetic activity to the bladder (pelvic nerve activity) and this coincides with periods of phasic bladder contractions. In recent studies, we have shown that regions of the CNS that modulate pelvic nerve activity also affect cardiovascular variables. Recent anatomical studies have shown neuronal connections between the areas of the CNS that modulate both reflexes. Accordingly, in the present study we investigate if during the Bezold-Jarisch reflex there are simultaneous changes in pelvic nerve activity. METHODS: Experiments were performed in Wistar female rats, anaesthetised with alpha-chloradose i.p. (80 micrograms/Kg) supplemented i.v. as required. Arterial blood pressure, ECG heart rate, urinary bladder pressure and pelvic nerve activity were recorded. RESULTS: Stimulation of cardiac chemosensitive nerve endings with veratridine evoked a decrease in arterial blood pressure from 88.6 +/- 1.72 to 66.1 +/- 2.50 mmHg (n = 30; p < 0.0001) and of heart rate from 420.3 +/- 5.56 to 248.8 +/- 17.58 bpm (n = 13; p < 0.0001) There were simultaneous changes of pelvic nerve activity that preceded an increase in urinary bladder pressure from 10.2 +/- 0.28 to 26.3 +/- 1.52 cmH2O (n = 30; p < 0.0001) and bladder contractions. We believe that the reflex changes resulted from activation of cardiac chemosensory nerve endings, as equivalent injections of warm saline into the left ventricle produced no changes in either cardiovascular variables or pelvic nerve activity. CONCLUSIONS: These observations suggest a significant role for cardiac afferents in modulating bladder contractions. The integration and functional significance of these inputs remain to be elucidated. The clinical importance of this physiological result may contribute to a better understanding of the mechanism of some semiologic findings, notably the association of urgency to micturate with myocardial ischemia and myocardial infarction.

Animals↗
PubMed1999

Identification of neural projections from the forebrain to the kidney, using the virus pseudorabies.

These data demonstrate a chain of synaptically connected neurons extending to the rat kidney through several levels of the neuraxis from the forebrain, and the lamina terminalis -- an area known to be involved in the regulation of body fluid homeostasis. The Bartha strain of pseudorabies virus was injected into the kidney of male Sprague-Dawley rats, resulting in retrograde infections in spinal cord segments (T1-T8), and successive infection in five autonomic 'premotor' areas of the brain, the rostroventrolateral medulla, rostroventromedial medulla, raphe nuclei, A5 region of the pons, and the paraventricular nucleus of the hypothalamus, as well as the nucleus of the solitary tract, locus coeruleus, and subcoeruleus nuclei. Higher order labelling was found in regions of the forebrain, including the organum vasculosum of the lamina terminalis, median preoptic nucleus, subfornical organ, medial preoptic area, bed nucleus of the stria terminalis, anteroventral periventricular nucleus, lateral preoptic area, suprachiasmatic nucleus, retrochiasmatic nucleus, primary motor cortex, and visceral cortex. This polysynaptic pathway to the kidney may form the substrate underlying the impact of forebrain structures on renal function.

Journal Article↗
PubMed2002

Antagonistic effects of Rnd1 and RhoD GTPases regulate receptor activity in Semaphorin 3A-induced cytoskeletal collapse.

The semaphorins are a large protein family that is involved in the patterning of neuronal connections in the developing nervous system of both vertebrates and invertebrates. The chemorepulsive axon guidance signal Semaphorin 3A (Sema3A) induces the depolymerization of actin filaments and the collapse of sensory growth cones by activating a receptor complex that contains a plexin as the signal-transducing subunit. Here we show that, of a large number of GTPases tested, only Rnd1 and RhoD bind the cytoplasmic domain of Plexin-A1. Recruitment of active Rnd1 is sufficient to trigger signaling by Plexin-A1, even in the absence of Sema3A, and initiates cytoskeletal collapse by activating its cytoplasmic domain. RhoD, in contrast, blocks Plexin-A1 activation by Rnd1 and repulsion of sympathetic axons by Sema3A. Thus, the antagonism of two GTPases regulates the activity of the Sema3A receptor, and activation by Rnd1 appears to be an essential step in signaling by Plexin-A1.

Animals↗
PubMed2002

Local and target-derived brain-derived neurotrophic factor exert opposing effects on the dendritic arborization of retinal ganglion cells in vivo.

The dendritic and axonal arbors of developing retinal ganglion cells (RGCs) are exposed to two sources of BDNF: RGC dendrites are exposed to BDNF locally within the retina, and RGC axons are exposed to BDNF at the target, the optic tectum. Our previous studies demonstrated that increasing tectal BDNF levels promotes RGC axon terminal arborization, whereas increasing retinal BDNF levels inhibits RGC dendritic arborization. These results suggested that differential neurotrophic action at the axon versus dendrite might be responsible for the opposing effects of BDNF on RGC axonal versus dendritic arborization. To explore this possibility, we examined the effects of altering BDNF levels at the optic tectum on the elaboration of RGC dendritic arbors in the retina. Increasing tectal BDNF levels resulted in a significant increase in dendritic branching, whereas neutralizing endogenous tectal BDNF with function-blocking antibodies significantly decreased dendritic arbor complexity. Thus, RGC dendritic arbors react in opposing manners to retinal- versus tectal-derived BDNF. Alterations in retinal BDNF levels, however, did not affect axon terminal arborization. Thus, RGC dendritic arborization is controlled in a complementary manner by both local and target-derived sources of BDNF, whereas axon arborization is modulated solely by neurotrophic interactions at the target. Together, our results indicate that developing RGCs modulate dendritic arborization by integrating signals from discrete sources of BDNF in the eye and brain. Differential integration of spatially discrete neurotrophin signals within a single neuron may therefore finely tune afferent and efferent neuronal connectivity.

Animals↗
PubMed2003

[Electroretinography in the diagnosis and study of pathogenesis of X-linkage retinoschizis].

Due to an extensive variability of manifestations of X-linkage retinoschizis, there is a need in a differential diagnosis of it and of other hereditary retinal diseases. The method of electroretinography is often of primary importance in specifying a diagnosis in ophthalmology; it both enables the detection of new and more sensitive criteria of early and differential diagnosis and ensures a more profound understanding of changes occurring in the retina. A topical analysis of changes of the bioelectric activity taking place in different retinal layers and sections as well as a differential evaluation of the functional condition of neurons and glia Muller's cells in patients with X-linkage retinoschizis were accomplished within the framework of this study. The nature of the peak latency and of the b-wave amplitude in the electroretinogram (ERG) and in the mechano-electroretinogram (MERG) as well as of a low-frequency ERG is indicative of that Muller's cells are damaged; the damage severity is related with an intensity of the pathological process and can be objectively determined by the ERG examinations of patients. An analysis of sub-components of a low-frequency rheoelectroretinogram (RERG) shows weakened inhibitory inter-neuron connections in the retina, which is a sign of disease aggravation. The regularities of changes of retinal biopotential to blue light flashes under all registration conditions (ganz-feld, macular and rhythmical stimulation) differ from the ERG dynamics to other light stimuli, which is indicative of a significant role of the pathology of S-cone paths in the development of X-linkage retinoschizis.

Adolescent↗
PubMed2003

Melanocytes: morphological basis for an exteroceptive sensory system for monitoring ultraviolet radiation.

From the conventional medical perspective, melanocytes have been traditionally viewed as epidermal responders/reactors to ultraviolet radiation. In this paper we have begun an analysis of the functional significance of melanocytes as monitors for ultraviolet radiation with their neuronal, endocrinological and immunological intercalations. This preliminary study was performed using as a human model unilateral sural nerve sensory blockade before and after ultraviolet exposure to both feet while the unblocked foot acted as the control. Full thickness surgical skin biopsies were taken of (I), normal pre-exposure skin, in the center of the two centimeter exposure area of both the sural nerve blocked area (II-III) and control (IV-V) one centimeter outside the exposed area in both the sural nerve blocked foot and the control or non-blocked foot. The objective clinical, blinded morphological and immuno-histochemical data from this experiment support the initial conclusion that neuronal connection is necessary for the normal ultraviolet exposure dermal reaction. Based upon this study, we further propose the existence of an exteroceptive sensory system in which melanocytes, with direct nervous system connection initiate an ultraviolet radiation reactive response that mobilizes both conventional endocrine and immune pathways.

Cell Shape↗
PubMed2004

Molecular mechanisms of brain plasticity: neurophysiologic and neuroimaging studies in the developing patients.

The term plasticity, derived from the Greek word "plaistikos" meaning "to form" refers to the brain's ability to learn, remember and forget as well as its capacity to reorganize and recover from injury. There are four major types of plasticity: adaptive plasticity, impaired plasticity, excessive plasticity, and the 'Achilles heel' of the developing brain. Mechanisms of plasticity include: a change in the balance of excitation and inhibition; a long-term potentiation (LTP) or long-term depression (LTD); a change in neuronal membrane excitability; the anatomical changes-formation of new axon terminals and new synapses. Mechanisms for plasticity include activity-dependent refinement of neuronal connections and synaptic plasticity as a substrate for learning and memory. The molecular mechanisms for these processes were described in view of the current investigations. Authors presented: the role of calcium ions, calcium channels, NMDA receptors, free radicals, lipid peroxides and neurotrophins in the plasticity of developing brain. The utility of the neurophysiologic and MRI techniques were described in the determination of brain reorganization and repair in patients with cerebral palsy. Authors discussed their results on quantitative EEG and spectroscopy MRI studies in children with cerebral palsy. They have shown the existence of two processes in brain: brain damage and recovery.

Brain↗
PubMed2005

[The clinical utility of MR diffusion tensor imaging and spatially normalized PET to evaluate traumatic brain injury patients with memory and cognitive impairments].

We detected and compared abnormal brain areas using both MR diffusion tensor imaging (DTI) and easy Z score imaging system (eZIS) of FDG-PET for traumatic brain injury patients with memory and cognitive impairments. Twenty normal subjects and eighteen diffuse axonal injury patients with memory and cognitive impairments were studied with DTI and eZIS of 18F-FDG-PET. DTI contained fractional anisotorophy (FA) analysis and the tractography for the corpus callosum. After PET imaging was performed, statistical analysis using eZIS was undergone with followed processing steps, including smoothing, normalization and z transformation with respect to normal database. Z score map was superimposed on 3D MRI brain. Group analysis was performed using SPM. In diffuse axonal injury patients, the decline of FA was observed around the corpus callosum in comparison with normal subjects and the reduction of glucose metabolism was shown in the cingulated association. These results suggest that the reduction of metabolism within the cingulated cortex indicated deprived neuronal activation caused by the impaired neuronal connectivity that was revealed with DTI. Furthermore, the metabolic abnormalities within the cingulated cortex may be responsible for memory and cognitive impairments. DTI and spatially normalized PET have a role in neuroimaging interpretation for patients with memory and cognition impairments because its 3D better visualization allows objective and systematic investigation.

Accidents, Traffic↗