Peripheral nerve induces macrophage neurotrophic activities: regulation of neuronal process outgrowth, intracellular signaling and synaptic function

2003 ◽  
Vol 142 (1-2) ◽  
pp. 112-129 ◽  
Author(s):  
Annemarie Shibata ◽  
Marina Zelivyanskaya ◽  
Jenae Limoges ◽  
Kimberly A Carlson ◽  
Santhi Gorantla ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Intracellular Signaling ◽  
Synaptic Function ◽  
Neuronal Process ◽  
Process Outgrowth

scholarly journals Thyroid Hormones and Peripheral Nerve Regeneration

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Ioannis D. Papakostas ◽  
George A. Macheras
Keyword(s):  
Thyroid Hormone ◽  
Peripheral Nerve ◽  
Nerve Regeneration ◽  
Intracellular Signaling ◽  
Peripheral Nerve Regeneration ◽  
Tissue Growth ◽  
Tissue Response ◽  
Cell Integrity ◽  
Neuronal Soma ◽  
Insight Into

Peripheral nerve regeneration is a unique process in which cellular rather than tissue response is involved. Depending on the extent and proximity of the lesion and the age and type of the neuronal soma, the cell body may either initiate a reparative response or may die. Microsurgical intervention may alter the prognosis after a peripheral nerve injury but to a certain extent. By altering the biochemical microenvironment of the neuron, we can increase the proportion of neurons that survive the injury and initiate the reparative response. Thyroid hormone critically regulates tissue growth and differentiation and plays a crucial role during organ development. Furthermore, recent research has provided new insight into thyroid hormone cellular action. Thyroid hormone regulates stress response intracellular signaling and targets molecules important for cytoskeletal stability and cell integrity. Changes in thyroid hormone signaling occur in nerve and other tissues, with important physiological consequences. The interest in thyroid hormone in the context of nerve regeneration has recently been revived.

N-cadherin and integrins: Two receptor systems that mediate neuronal process outgrowth on astrocyte surfaces

Neuron ◽  
1988 ◽  
Vol 1 (1) ◽  
pp. 33-43 ◽  
Author(s):  
Kevin J. Tomaselli ◽  
Karla M. Neugebauer ◽  
John L. Bixby ◽  
Jack Lilien ◽  
Louis F. Reichard
Keyword(s):  
Neuronal Process ◽  
Process Outgrowth

scholarly journals Distinct molecular interactions mediate neuronal process outgrowth on non-neuronal cell surfaces and extracellular matrices.

1986 ◽  
Vol 103 (6) ◽  
pp. 2659-2672 ◽  
Author(s):  
K J Tomaselli ◽  
L F Reichardt ◽  
J L Bixby
Keyword(s):  
Cell Surface ◽  
Neurite Outgrowth ◽  
Schwann Cells ◽  
Neuronal Cell ◽  
Extracellular Matrices ◽  
Cell Surfaces ◽  
Neuronal Process ◽  
Promote Neurite Outgrowth ◽  
Process Outgrowth ◽  
Skeletal Myotubes

We have compared neurite outgrowth on extracellular matrix (ECM) constituents to outgrowth on glial and muscle cell surfaces. Embryonic chick ciliary ganglion (CG) neurons regenerate neurites rapidly on surfaces coated with laminin (LN), fibronectin (FN), conditioned media (CM) from several non-neuronal cell types that secrete LN, and on intact extracellular matrices. Neurite outgrowth on all of these substrates is blocked by two monoclonal antibodies, CSAT and JG22, that prevent the adhesion of many cells, including neurons, to the ECM constituents LN, FN, and collagen. Neurite outgrowth is inhibited even on mixed LN/poly-D-lysine substrates where neuronal attachment is independent of LN. Therefore, neuronal process outgrowth on extracellular matrices requires the function of neuronal cell surface molecules recognized by these antibodies. The surfaces of cultured astrocytes, Schwann cells, and skeletal myotubes also promote rapid process outgrowth from CG neurons. Neurite outgrowth on these surfaces, though, is not prevented by CSAT or JG22 antibodies. In addition, antibodies to a LN/proteoglycan complex that block neurite outgrowth on several LN-containing CM factors and on an ECM extract failed to inhibit cell surface-stimulated neurite outgrowth. After extraction with a nonionic detergent, Schwann cells and myotubes continue to support rapid neurite outgrowth. However, the activity associated with the detergent insoluble residue is blocked by CSAT and JG22 antibodies. Detergent extraction of astrocytes, in contrast, removes all neurite-promoting activity. These results provide evidence for at least two types of neuronal interactions with cells that promote neurite outgrowth. One involves adhesive proteins present in the ECM and ECM receptors on neurons. The second is mediated through detergent-extractable macromolecules present on non-neuronal cell surfaces and different, uncharacterized receptor(s) on neurons. Schwann cells and skeletal myotubes appear to promote neurite outgrowth by both mechanisms.

scholarly journals Myosin IIC: A Third Molecular Motor Driving Neuronal Dynamics

2008 ◽  
Vol 19 (9) ◽  
pp. 3956-3968 ◽  
Author(s):  
Steven R. Wylie ◽  
Peter D. Chantler
Keyword(s):  
Molecular Motors ◽  
Molecular Motor ◽  
Neuronal Cell ◽  
Neuronal Dynamics ◽  
Neuronal Process ◽  
Process Outgrowth ◽  
Myosin Iia ◽  
Neuronal Adhesion ◽  
Functional Knockdown ◽  
Distinctive Phenotype

Neuronal dynamics result from the integration of forces developed by molecular motors, especially conventional myosins. Myosin IIC is a recently discovered nonsarcomeric conventional myosin motor, the function of which is poorly understood, particularly in relation to the separate but coupled activities of its close homologues, myosins IIA and IIB, which participate in neuronal adhesion, outgrowth and retraction. To determine myosin IIC function, we have applied a comparative functional knockdown approach by using isoform-specific antisense oligodeoxyribonucleotides to deplete expression within neuronally derived cells. Myosin IIC was found to be critical for driving neuronal process outgrowth, a function that it shares with myosin IIB. Additionally, myosin IIC modulates neuronal cell adhesion, a function that it shares with myosin IIA but not myosin IIB. Consistent with this role, myosin IIC knockdown caused a concomitant decrease in paxillin-phospho-Tyr118 immunofluorescence, similar to knockdown of myosin IIA but not myosin IIB. Myosin IIC depletion also created a distinctive phenotype with increased cell body diameter, increased vacuolization, and impaired responsiveness to triggered neurite collapse by lysophosphatidic acid. This novel combination of properties suggests that myosin IIC must participate in distinctive cellular roles and reinforces our view that closely related motor isoforms drive diverse functions within neuronal cells.

D1/D5 Dopamine Receptors Stimulate Intracellular Calcium Release in Primary Cultures of Neocortical and Hippocampal Neurons

2002 ◽  
Vol 87 (4) ◽  
pp. 2167-2175 ◽  
Author(s):  
Nelson Lezcano ◽  
Clare Bergson
Keyword(s):  
Intracellular Calcium ◽  
Dopamine Receptors ◽  
Intracellular Signaling ◽  
Hippocampal Neurons ◽  
Calcium Release ◽  
Neuronal Excitability ◽  
Primary Cultures ◽  
Synaptic Function ◽  
State Dependent ◽  
Camp Levels

D1/D5 dopamine receptors in basal ganglia, hippocampus, and cerebral cortex modulate motor, reward, and cognitive behavior. Previous work with recombinant proteins revealed that in cells primed with heterologous Gq/11-coupled G-protein-coupled receptor (GPCR) agonists, the typically Gs-linked D1/D5 receptors can stimulate robust release of calcium from internal stores when coexpressed with calcyon. To learn more about the intracellular signaling mechanisms underlying these D1/D5 receptor regulated behaviors, we explored the possibility that endogenous receptors stimulate internal release of calcium in neurons. We have identified a population of neurons in primary cultures of hippocampus and neocortex that respond to D1/D5 dopamine receptor agonists with a marked increase in intracellular calcium (Ca[Formula: see text]) levels. The D1/D5 receptor stimulated responses occurred in the absence of extracellular Ca2+ indicating the rises in Ca[Formula: see text] involve release from internal stores. In addition, the responses were blocked by D1/D5 receptor antagonists. Further, the D1/D5 agonist-evoked responses were state dependent, requiring priming with agonists of Gq/11-coupled glutamate, serotonin, muscarinic, and adrenergic receptors or with high external K+solution. In contrast, D1/D5 receptor agonist-evoked Ca2+ responses were not detected in neurons derived from striatum. However, D1/D5 agonists elevated cAMP levels in striatal cultures as effectively as in neocortical and hippocampal cultures. Further, neither forskolin nor 8-Br-cAMP stimulation following priming was able to mimic the D1/D5 agonist-evoked Ca2+ response in neocortical neurons indicating that increased cAMP levels are not sufficient to stimulate Ca[Formula: see text] release. Our data suggest that D1-like dopamine receptors likely modulate neocortical and hippocampal neuronal excitability and synaptic function via Ca2+ as well as cAMP-dependent signaling.

scholarly journals Mitochondrial alarmins released by degenerating motor axon terminals activate perisynaptic Schwann cells

2015 ◽  
Vol 112 (5) ◽  
pp. E497-E505 ◽  
Author(s):  
Elisa Duregotti ◽  
Samuele Negro ◽  
Michele Scorzeto ◽  
Irene Zornetta ◽  
Bryan C. Dickinson ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Schwann Cells ◽  
Intracellular Signaling ◽  
Molecular Mechanisms ◽  
Mapk Pathway ◽  
Motor Axon ◽  
Nerve Terminals ◽  
Axon Terminals ◽  
Terminal Degeneration

An acute and highly reproducible motor axon terminal degeneration followed by complete regeneration is induced by some animal presynaptic neurotoxins, representing an appropriate and controlled system to dissect the molecular mechanisms underlying degeneration and regeneration of peripheral nerve terminals. We have previously shown that nerve terminals exposed to spider or snake presynaptic neurotoxins degenerate as a result of calcium overload and mitochondrial failure. Here we show that toxin-treated primary neurons release signaling molecules derived from mitochondria: hydrogen peroxide, mitochondrial DNA, and cytochrome c. These molecules activate isolated primary Schwann cells, Schwann cells cocultured with neurons and at neuromuscular junction in vivo through the MAPK pathway. We propose that this inter- and intracellular signaling is involved in triggering the regeneration of peripheral nerve terminals affected by other forms of neurodegenerative diseases.

scholarly journals α-COP binding to the survival motor neuron protein SMN is required for neuronal process outgrowth

2015 ◽  
Vol 24 (25) ◽  
pp. 7295-7307 ◽  
Author(s):  
Hongxia Li ◽  
Sara K. Custer ◽  
Timra Gilson ◽  
Le Thi Hao ◽  
Christine E. Beattie ◽  
...  
Keyword(s):  
Motor Neuron ◽  
Survival Motor Neuron ◽  
Neuronal Process ◽  
Survival Motor Neuron Protein ◽  
Motor Neuron Protein ◽  
Process Outgrowth

scholarly journals Glucocorticoid Prevents Brain-Derived Neurotrophic Factor-Mediated Maturation of Synaptic Function in Developing Hippocampal Neurons through Reduction in the Activity of Mitogen-Activated Protein Kinase

2008 ◽  
Vol 22 (3) ◽  
pp. 546-558 ◽  
Author(s):  
Emi Kumamaru ◽  
Tadahiro Numakawa ◽  
Naoki Adachi ◽  
Yuki Yagasaki ◽  
Aiko Izumi ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Neurotrophic Factor ◽  
Intracellular Signaling ◽  
Hippocampal Neurons ◽  
Glutamate Release ◽  
Brain Derived Neurotrophic Factor ◽  
Synaptic Function ◽  
Synaptic Proteins ◽  
Mature Stage ◽  
Synaptic Maturation

Abstract An increased level of glucocorticoid may be related to the pathophysiology of depressive disorder. The involvement of brain-derived neurotrophic factor (BDNF) in the antidepressive effect has also been suggested; however, the possible influence of glucocorticoid on the action of BDNF in the developing central nervous system has not been elucidated. In this study, we investigated the effect of glucocorticoid (dexamethasone, DEX) on synaptic maturation and function enhanced by BDNF in early developing hippocampal neurons. In the immature stage, BDNF increased the outgrowth of dendrites and the expression of synaptic proteins including glutamate receptors and presynaptic proteins. Pretreatment with DEX significantly inhibited the BDNF-dependent up-regulation of both dendritic outgrowth and synaptic proteins. In the more mature stage, the BDNF-reinforced postsynaptic Ca2+ influx was decreased by DEX. BDNF-enhanced presynaptic glutamate release was also suppressed. RU486, a glucocorticoid receptor antagonist, canceled the DEX-dependent blocking effect on the action of BDNF. After down-regulation of glucocorticoid receptor by small interfering RNA application, no inhibitory effect of DEX on the BDNF-increased synaptic proteins was observed. Interestingly, the BDNF-activated MAPK/ERK pathway, which is an essential intracellular signaling pathway for the BDNF-increased synaptic proteins, was reduced by DEX. These results suggest that BDNF-mediated synaptic maturation is disturbed after neurons are exposed to high-level glucocorticoid in their development stage.

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