scholarly journals One Raft to Guide Them All, and in Axon Regeneration Inhibit Them

2021 ◽  
Vol 22 (9) ◽  
pp. 5009
Author(s):  
Marc Hernaiz-Llorens ◽  
Ramón Martínez-Mármol ◽  
Cristina Roselló-Busquets ◽  
Eduardo Soriano
Keyword(s):  
Nervous System ◽  
Neuronal Cell ◽  
Neuronal Cell Body ◽  
Central Nervous System Damage ◽  
Surgical Interventions ◽  
Traumatic Injuries ◽  
Functional Connections ◽  
Molecular Machinery ◽  
The Stability ◽  
Lipid Raft Microdomains

Central nervous system damage caused by traumatic injuries, iatrogenicity due to surgical interventions, stroke and neurodegenerative diseases is one of the most prevalent reasons for physical disability worldwide. During development, axons must elongate from the neuronal cell body to contact their precise target cell and establish functional connections. However, the capacity of the adult nervous system to restore its functionality after injury is limited. Given the inefficacy of the nervous system to heal and regenerate after damage, new therapies are under investigation to enhance axonal regeneration. Axon guidance cues and receptors, as well as the molecular machinery activated after nervous system damage, are organized into lipid raft microdomains, a term typically used to describe nanoscale membrane domains enriched in cholesterol and glycosphingolipids that act as signaling platforms for certain transmembrane proteins. Here, we systematically review the most recent findings that link the stability of lipid rafts and their composition with the capacity of axons to regenerate and rebuild functional neural circuits after damage.

scholarly journals Common Structural Lesions of the Peripheral Nervous System

2019 ◽  
Vol 48 (1) ◽  
pp. 96-104 ◽  
Author(s):  
Bernard S. Jortner
Keyword(s):  
Nervous System ◽  
Schwann Cell ◽  
Peripheral Nerve ◽  
Structural Changes ◽  
Neuronal Cell ◽  
Neuronal Cell Body ◽  
Primary Target ◽  
Toxic Neuropathy ◽  
Reciprocal Influences ◽  
Primary Injury

This review illustrates common lesions of peripheral nerve myelinated fibers that occur in toxic neuropathy. These distinctive structural changes help to define the site of toxicant activity and thus predict the course of neurotoxic disease and recovery. Neuronopathy is the condition where the primary injury is directed to the neuronal cell body giving rise to a peripheral nerve axon. Axonopathy occurs when the axon is the primary target, and myelinopathy develops where the Schwann cell and/or myelin sheath is the primary target; these conditions can be discriminated early during the course of nerve fiber degeneration, but reciprocal influences between axon and myelin result in degeneration of both structures late in the disease.

scholarly journals The Extracellular Environment of the CNS: Influence on Plasticity, Sprouting, and Axonal Regeneration after Spinal Cord Injury

2018 ◽  
Vol 2018 ◽  
pp. 1-18 ◽  
Author(s):  
Shmma Quraishe ◽  
Lindsey H. Forbes ◽  
Melissa R. Andrews
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Axonal Regeneration ◽  
Neuronal Cell ◽  
Developmental State ◽  
Neuronal Cell Body ◽  
Mature Adult ◽  
Cord Injury ◽  
Extracellular Environment

The extracellular environment of the central nervous system (CNS) becomes highly structured and organized as the nervous system matures. The extracellular space of the CNS along with its subdomains plays a crucial role in the function and stability of the CNS. In this review, we have focused on two components of the neuronal extracellular environment, which are important in regulating CNS plasticity including the extracellular matrix (ECM) and myelin. The ECM consists of chondroitin sulfate proteoglycans (CSPGs) and tenascins, which are organized into unique structures called perineuronal nets (PNNs). PNNs associate with the neuronal cell body and proximal dendrites of predominantly parvalbumin-positive interneurons, forming a robust lattice-like structure. These developmentally regulated structures are maintained in the adult CNS and enhance synaptic stability. After injury, however, CSPGs and tenascins contribute to the structure of the inhibitory glial scar, which actively prevents axonal regeneration. Myelin sheaths and mature adult oligodendrocytes, despite their important role in signal conduction in mature CNS axons, contribute to the inhibitory environment existing after injury. As such, unlike the peripheral nervous system, the CNS is unable to revert to a “developmental state” to aid neuronal repair. Modulation of these external factors, however, has been shown to promote growth, regeneration, and functional plasticity after injury. This review will highlight some of the factors that contribute to or prevent plasticity, sprouting, and axonal regeneration after spinal cord injury.

scholarly journals Serotonin release from the neuronal cell body and its long-lasting effects on the nervous system

2015 ◽  
Vol 370 (1672) ◽  
pp. 20140196 ◽  
Author(s):  
Francisco F. De-Miguel ◽  
Carolina Leon-Pinzon ◽  
Paula Noguez ◽  
Bruno Mendez
Keyword(s):  
Nervous System ◽  
Cell Body ◽  
Calcium Release ◽  
Neuronal Cell ◽  
Serotonin Release ◽  
Neuronal Cell Body ◽  
Neuronal Cell Bodies ◽  
Multistep Process ◽  
The Central Nervous System ◽  
Calcium Induced Calcium Release

Serotonin, a modulator of multiple functions in the nervous system, is released predominantly extrasynaptically from neuronal cell bodies, axons and dendrites. This paper describes how serotonin is released from cell bodies of Retzius neurons in the central nervous system (CNS) of the leech, and how it affects neighbouring glia and neurons. The large Retzius neurons contain serotonin packed in electrodense vesicles. Electrical stimulation with 10 impulses at 1 Hz fails to evoke exocytosis from the cell body, but the same number of impulses at 20 Hz promotes exocytosis via a multistep process. Calcium entry into the neuron triggers calcium-induced calcium release, which activates the transport of vesicle clusters to the plasma membrane. Exocytosis occurs there for several minutes. Serotonin that has been released activates autoreceptors that induce an inositol trisphosphate-dependent calcium increase, which produces further exocytosis. This positive feedback loop subsides when the last vesicles in the cluster fuse and calcium returns to basal levels. Serotonin released from the cell body is taken up by glia and released elsewhere in the CNS. Synchronous bursts of neuronal electrical activity appear minutes later and continue for hours. In this way, a brief train of impulses is translated into a long-term modulation in the nervous system.

The Red Neuronal Pigment in the Nervous System of the Mussel, Mytilus Edulis: Localization and Its Effect on Lateral Ciliary Activity with Spectral and Analytical Changes

1981 ◽  
Vol 39 ◽  
pp. 494-495
Author(s):  
Anthony A. Paparo ◽  
Judith A. Murphy
Keyword(s):  
Nervous System ◽  
Mytilus Edulis ◽  
Neuronal Cell ◽  
Ciliary Activity ◽  
Neuronal Cell Bodies ◽  
The Central Nervous System ◽  
Intracellular Organelles ◽  
The Common ◽  
The Individual ◽  
Cryostat Sections

The purpose of this study was to localize the red neuronal pigment in Mytilus edulis and examine its role in the control of lateral ciliary activity in the gill. The visceral ganglia (Vg) in the central nervous system show an over al red pigmentation. Most red pigments examined in squash preps and cryostat sec tions were localized in the neuronal cell bodies and proximal axon regions. Unstained cryostat sections showed highly localized patches of this pigment scattered throughout the cells in the form of dense granular masses about 5-7 um in diameter, with the individual granules ranging from 0.6-1.3 um in diame ter. Tissue stained with Gomori's method for Fe showed bright blue granular masses of about the same size and structure as previously seen in unstained cryostat sections.Thick section microanalysis (Fig.l) confirmed both the localization and presence of Fe in the nerve cell. These nerve cells of the Vg share with other pigmented photosensitive cells the common cytostructural feature of localization of absorbing molecules in intracellular organelles where they are tightly ordered in fine substructures.

Brain organoids: a promising model to assess oxidative stress‐induced Central Nervous System damage

2021 ◽  
Author(s):  
Foluwasomi A. Oyefeso ◽  
Alysson R. Muotri ◽  
Christopher G. Wilson ◽  
Michael J. Pecaut
Keyword(s):  
Oxidative Stress ◽  
Central Nervous System ◽  
Nervous System ◽  
Central Nervous System Damage

scholarly journals Troublesome Heterotopic Ossification after Central Nervous System Damage: A Survey of 570 Surgeries

PLoS ONE ◽  
2011 ◽  
Vol 6 (1) ◽  
pp. e16632 ◽  
Author(s):  
François Genêt ◽  
Claire Jourdan ◽  
Alexis Schnitzler ◽  
Christine Lautridou ◽  
Didier Guillemot ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Heterotopic Ossification ◽  
Central Nervous System Damage

Initial characterization of anosmin-1, a putative extracellular matrix protein synthesized by definite neuronal cell populations in the central nervous system

1996 ◽  
Vol 109 (7) ◽  
pp. 1749-1757 ◽  
Author(s):  
N. Soussi-Yanicostas ◽  
J.P. Hardelin ◽  
M.M. Arroyo-Jimenez ◽  
O. Ardouin ◽  
R. Legouis ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Extracellular Matrix ◽  
Nervous System ◽  
Cell Membrane ◽  
Heparan Sulfate ◽  
Matrix Protein ◽  
Neuronal Cell ◽  
Extracellular Matrix Protein ◽  
Cell Populations

The KAL gene is responsible for the X-chromosome linked form of Kallmann's syndrome in humans. Upon transfection of CHO cells with a human KAL cDNA, the corresponding encoded protein, KALc, was produced. This protein is N-glycosylated, secreted in the cell culture medium, and is localized at the cell surface. Several lines of evidence indicate that heparan-sulfate chains of proteoglycan(s) are involved in the binding of KALc to the cell membrane. Polyclonal and monoclonal antibodies to the purified KALc were generated. They allowed us to detect and characterize the protein encoded by the KAL gene in the chicken central nervous system at late stages of embryonic development. This protein is synthesized by definite neuronal cell populations including Purkinje cells in the cerebellum, mitral cells in the olfactory bulbs and several subpopulations in the optic tectum and the striatum. The protein, with an approximate molecular mass of 100 kDa, was named anosmin-1 in reference to the deficiency of the sense of smell which characterizes the human disease. Anosmin-1 is likely to be an extracellular matrix component. Since heparin treatment of cell membrane fractions from cerebellum and tectum resulted in the release of the protein, we suggest that one or several heparan-sulfate proteoglycans are involved in the binding of anosmin-1 to the membranes in vivo.

Analysis of demographics and outcomes of surgical resection in the CNS of patients with melanoma.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e21534-e21534
Author(s):  
Achuta Kumar Guddati ◽  
Takefumi Komiya ◽  
Picon Hector ◽  
Allan N. Krutchik ◽  
Gagan Kumar
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Hospital Mortality ◽  
Surgical Resection ◽  
Home Healthcare ◽  
Teaching Hospitals ◽  
Surgical Interventions ◽  
Discharge Disposition ◽  
Nationwide Inpatient Sample Database ◽  
Significant Difference

e21534 Background: Patients with melanoma frequently develop central nervous system metastases. Oligometastatic disease is often treated either by surgical resection or by stereotactic radiotherapy. This study investigates the trends and clinical outcomes of patients with melanoma who have undergone surgical procedures on the central nervous system during their hospitalization. Methods: A retrospective cohort study was performed based on admissions of adult patients who underwent craniectomy/surgical resection for metastatic melanoma from 2002 -2014 using the Nationwide Inpatient Sample database. The primary outcome measure was all-cause in-hospital mortality. Secondary outcomes included length of hospital stay(LOS) and discharge disposition (home/home with health care and skilled nursing facilities/long term acute care (SNF/LTAC)). Factors associated with in-hospital mortality were examined by multivariable logistic regression. We adjusted for patient and hospital characteristics, payer, and comorbid conditions. We also examined trends of mortality for the study years. P was kept at 0.05. Results: There were an estimated 5972 discharges of patients with melanoma undergoing craniectomy/surgical resection during the study period. Patients undergoing surgical interventions were typically males (69%) and whites (79%). 98% of procedures were performed at teaching hospitals. Unadjusted all-cause in-hospital mortality was 3.1%. There was no significant difference in mortality over 13 years. Age, gender, and race were not associated with increased in-hospital mortality. Median LOS was 5 days (IQR 3-9 days). LOS was longer in elderly and those with higher Charlson co-morbid index. Of the survivors, 76% were discharged to home or with home healthcare while 24% were discharged to SNF/LTAC. Patients with age > 65 (OR 2.9; 95%CI 2.2-3.9, p < 0.001) and those with higher Charlson co-morbid index (OR 1.2; 95%CI 1.1-1.3) had higher odds for being discharged to SNF/LTAC. Conclusions: Patients who undergo craniectomy/surgical resection for melanoma have a low in-hospital mortality rate. One quarter of patients are discharged to SNF/LTAC.

Neurotransmission in neonatal rat cardiac ganglion in situ

1990 ◽  
Vol 259 (4) ◽  
pp. H997-H1005 ◽  
Author(s):  
G. R. Seabrook ◽  
L. A. Fieber ◽  
D. J. Adams
Keyword(s):  
Neuronal Cell ◽  
Nerve Fibers ◽  
Heart Beat ◽  
Neonatal Rat ◽  
Neuronal Cell Body ◽  
High Frequency Stimulation ◽  
Excitatory Postsynaptic Potential ◽  
Cardiac Ganglion ◽  
Cardiac Ganglia

The intrinsic cardiac ganglia of the neonatal rat heart in situ were studied using electrophysiological and histochemical techniques. The vagal branches innervating the atrial myocardium and cardiac ganglia were identified and individual ganglion cells visualized using Hoffman modulation contrast optics. Histochemical studies revealed the presence of acetylcholinesterase activity associated with neuronal cell bodies and fibers, catecholamine-containing, small intensely fluorescent cells, and cell bodies and nerve fibers immunoreactive for vasoactive intestinal polypeptide. Intracellular recordings from the "principal" cells of the rat cardiac ganglion in situ revealed a fast excitatory postsynaptic potential (EPSP) evoked after electrical stimulation of the vagus nerve, which was inhibited by the nicotinic receptor antagonist, mecamylamine. No spontaneously firing neurons were found, although infrequent (less than 2 min-1) spontaneous miniature EPSPs were observed in most neurons. The quantal content of neurally evoked responses was between 10 and 30 quanta, and the presence of multiple EPSPs in some cells suggested polyneuronal innervation. The neurally evoked EPSP amplitude was dependent on the rate of nerve stimulation, decreasing with increasing frequency of stimulation. Neurons exhibited a sustained depolarization during high frequency stimulation (greater than 1 Hz), and in approximately 15% of the cells a slow depolarization lasting 1-3 min was observed after a train of stimuli. The presence of catecholamine- and neuropeptide-containing neuronal cell body fibers in neonatal rat cardiac ganglia in situ, along with neurally evoked postsynaptic responses resistant to cholinergic ganglionic blockers, suggests a role for noncholinergic transmission in the regulation of the mammalian heart beat.

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